<?xml version="1.0" encoding="utf-8"?>
    <rss version="2.0">
      <channel xmlns:content="http://purl.org/rss/1.0/modules/content/">
        <title>Frontiers in Physiology | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/physiology</link>
        <description>RSS Feed for Frontiers in Physiology | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-10-26T04:29:02.205+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1993774</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1993774</link>
        <title><![CDATA[A cross-sectional comparison of five large language models in answering Chinese-language patient queries on visual field defects associated with brain diseases]]></title>
        <pubdate>2026-10-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Shenghe Li</author><author>Ling Wang</author><author>Xiaoyan Wang</author><author>Ligang Jiang</author><author>Weihua Yang</author><author>Lu Xie</author>
        <description><![CDATA[BackgroundVisual field defects associated with brain diseases may arise from stroke, intracranial space-occupying lesions, and other central visual pathway disorders. Patient questions often span symptom recognition, explanation of causes, care triage, treatment, and rehabilitation. Large language models may improve access to patient education. However, their accuracy, logic, coherence, safety, and content accessibility have not been compared under controlled conditions in this high-risk, interdisciplinary Chinese-language setting. This study aimed to compare the performance of five selected large language models across multiple dimensions.MethodsIn this cross-sectional study, 30 fixed Chinese-language questions, refined by experts and phrased from a patient perspective, were submitted to ChatGPT 5.6 Sol, DeepSeek V4 Flash, Gemini 3.7 Flash, Qwen 3.8 Max, and Kimi K3 through a unified application programming interface (API) client. Each model generated one response per question in an independent single-turn session, with web retrieval disabled and conversation history cleared. Three raters, blinded to model identity, independently scored 150 randomly presented responses from 1 to 5 for accuracy, logic, coherence, safety, and content accessibility. Response time, word count, non-space character count, sentence count, paragraph count, and table count were also recorded. Models were compared using the Friedman test followed by Bonferroni-adjusted Wilcoxon signed-rank tests. Inter-rater agreement was assessed using Kendall’s W. Correlations were assessed using Spearman analysis with Benjamini-Hochberg false discovery rate correction.ResultsAgreement among the three raters was high across all five dimensions (Kendall’s W = 0.820–0.844; all P < 0.001). The five models differed in accuracy, coherence, and content accessibility (P < 0.001, P < 0.001, and P = 0.001, respectively). No statistically significant between-model differences were observed in logic or safety (P = 0.247 and P = 0.061, respectively). ChatGPT 5.6 Sol had the highest median accuracy score [4.67 (interquartile range, 4.00–5.00)], and Kimi K3 had the highest median coherence score [4.50 (4.00–5.00)]. Both models had a median content accessibility score of 4.67 (4.00–5.00). Response time, response length, and text structure also differed among models. However, their correlations with expert quality scores were generally weak (|ρ| ≤ 0.279).ConclusionThe five large language models exhibited distinctly multidimensional performance when answering Chinese-language patient questions about visual field defects associated with brain diseases. No single model consistently performed best across all clinically relevant dimensions. These findings are specific to the model versions tested on 15 August 2026; stability across repeated generations was not assessed. Response speed, length, and structure cannot substitute for direct assessment of medical quality. The absence of a statistically significant difference in safety ratings under controlled conditions does not imply equivalent or adequate clinical safety. Large language models are better suited to supporting patient education and clinician-patient communication under clinical supervision than to making diagnostic or treatment decisions independently.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1945469</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1945469</link>
        <title><![CDATA[Functional analyses of Apis cerana cerana DnaJC28: a new biomarker for environmental stress]]></title>
        <pubdate>2026-10-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Guilin Li</author><author>Xinyi Zou</author><author>Shaojuan Yin</author><author>Yue Sun</author><author>Qianqian Wen</author>
        <description><![CDATA[Pollination by honeybees is vital for maintaining the health of both ecological and agricultural systems. However, honeybee health is often influenced by multiple environmental stresses. Therefore, identifying the key genes involved in stress responses and investigating the molecular mechanisms through which honeybees respond to environmental stress are crucial. In this study, we report that Apis cerana cerana DnaJC28 (AccDnaJC28) is a typical DnaJ protein belonging to the heat shock protein subfamily that contains a J domain and is localized in the cytoplasm. The mRNA levels of AccDnaJC28 were higher in the thorax than in other tissues and in 1-day-old workers than in bees at other developmental stages. Several environmental stressors induced the expression of AccDnaJC28. Functional analyses revealed that silencing AccDnaJC28 decreased the thermotolerance of A. cerana cerana, whereas its overexpression increased the survival of Drosophila S2 cells under heat stress. These results indicate the crucial role of AccDnaJC28 in the stress response and its potential suitability as a novel biomarker. Mechanistic analysis further revealed that knockdown of AccDnaJC28 reduced both the enzymatic activity of certain antioxidant enzymes and the expression levels of related antioxidant genes. In addition, the upregulated expression of certain antioxidant genes may partially compensate for the functional deficiency caused by AccDnaJC28 knockdown. Taken together, our findings demonstrate that AccDnaJC28 is essential for the response of A. cerana cerana to environmental stress, as it mitigates oxidative damage via the antioxidant signaling pathway. These results contribute to the understanding of the foundational defense mechanisms initiated by honeybees in response to environmental stress.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1983362</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1983362</link>
        <title><![CDATA[Trimethylamine N-oxide (TMAO) in heat stroke: molecular mechanisms from gut dysbiosis to multi-organ injury]]></title>
        <pubdate>2026-10-23T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Qiong Wu</author><author>Guodong Lin</author><author>Yuanyuan Ou</author><author>Bo Ji</author><author>Zhiguo Pan</author><author>Yu Shao</author>
        <description><![CDATA[Heat stroke, a life-threatening condition characterized by core hyperthermia (≥40 °C), central nervous system dysfunction, and multi-organ failure with mortality rates of 20–70%, is increasingly recognized as a systemic inflammatory and hemodynamic disorder rather than a purely thermoregulatory collapse. Among the emerging mediators of its pathophysiology, trimethylamine N-oxide (TMAO)—a gut microbiota-derived metabolite generated from dietary choline, L-carnitine, and betaine—has attracted growing attention as a molecular link between heat-induced gut dysbiosis and multi-organ injury. This review synthesizes current evidence on the physiological and molecular mechanisms whereby TMAO is proposed to aggravate heat stroke pathology, including: (1) NLRP3 inflammasome activation via ROS-TXNIP, SIRT3-SOD2-mtROS, and cathepsin B-mediated pathways; (2) endothelial dysfunction through tight junction disruption, eNOS/NO suppression, and ALDH2/ROS/GSDMD-dependent pyroptosis; (3) platelet hyperreactivity and thrombosis through enhanced Ca2+ mobilization and IP3 signaling; (4) mitochondrial oxidative stress and bioenergetic failure; and (5) neuroinflammation via the gut–brain axis. We further discuss the concentration-dependent duality of TMAO as a chemical chaperone versus a pathological mediator, and evaluate translational strategies targeting TMAO metabolism, including gut microbiota modulation, TMA lyase inhibition, and NLRP3 blockade. Importantly, the majority of the mechanistic evidence synthesized herein derives from disease models other than heat stroke (e.g., atherosclerosis, chronic kidney disease, obesity, aging, preeclampsia, and ischemic stroke); direct evidence obtained in heat-stroke settings remains limited, and several proposed pathways should be regarded as hypotheses awaiting heat-stroke-specific validation. Elucidating TMAO-dependent mechanisms may therefore inform future biomarker development and therapeutic investigation—both of which require clinical validation in heat-stroke patients—in this increasingly prevalent climate-sensitive disease.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1979863</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1979863</link>
        <title><![CDATA[Ocean acidification impairs embryonic development and disrupts ink sac gene expression in the pharaoh cuttlefish (Sepia pharaonis)]]></title>
        <pubdate>2026-10-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Shaogang Li</author><author>Jiawen Liang</author><author>Jiahe Liu</author><author>Yongsen Lv</author><author>Junhao Peng</author><author>Ming Zeng</author><author>Chunyan Guo</author><author>Haiyang Zhang</author><author>Jigui Yuan</author><author>Liyun Wang</author>
        <description><![CDATA[BackgroundOcean acidification (OA) represents a growing threat to marine biodiversity, particularly affecting the sensitive early life stages of invertebrates. While the physiological impacts of OA are widely recognized, its specific effects on organogenesis and the molecular regulation of defensive traits in cephalopods remain poorly understood. This study investigated the influence of acidified seawater on the embryonic development and ink sac formation in the Pharaoh cuttlefish (Sepia pharaonis).MethodsEmbryos were reared under four pH conditions (8.0, 7.7, 7.3, and 6.5). Embryonic growth, survival, hatching success, and ink sac morphogenesis were monitored throughout development. The expression of melanin synthesis–related genes, including tyr, per, and spNOS, was quantified using qRT-PCR.ResultsOcean acidification impaired embryonic development in a pH-dependent manner. Severe acidification (pH 6.5) resulted in complete mortality and no surviving embryos by Day 9, while moderate acidification (pH 7.3) led to delayed development and failure to hatch by Day 11, compared to the hatching observed in the control group. Ink sac development was markedly inhibited under acidified conditions, resulting in reduced size and pigmentation. Consistent with these morphological abnormalities, the expression of melanin synthesis markers, including tyrosinase (tyr) and peroxidase (per), exhibited a biphasic response, with early transient induction followed by consistent downregulation across all acidified treatments, while, the expression of the regulatory gene Sepia pharaonis nitric oxide synthase (spNOS) was significantly suppressed under severe acidification.ConclusionsThese findings provide evidence that OA is associated with disrupted embryogenesis and impaired ink sac formation in S. pharaonis, accompanied by altered expression of melanin synthesis-related genes. The resulting reduction in defensive capacity may increase the vulnerability of hatchlings and potentially affect population recruitment under future ocean acidification scenarios.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1945787</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1945787</link>
        <title><![CDATA[Edible insect-based feed ingredients as modulators of gastrointestinal physiology in monogastric livestock and aquaculture species]]></title>
        <pubdate>2026-10-23T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Oscar Abel Sánchez-Velázquez</author><author>Alan Javier Hernández-Álvarez</author>
        <description><![CDATA[Edible insects have emerged as promising sustainable feed ingredients capable of supporting both animal production and gastrointestinal health. Beyond their nutritional value, insect-derived meals contain bioactive compounds—including chitin, antimicrobial peptides, medium-chain fatty acids, micronutrients, and antioxidant molecules—that may modulate gut microbiota–host interactions in farmed monogastric animal species. This review critically examines current evidence on the mechanisms through which insect-based diets influence gastrointestinal physiology in livestock and aquaculture species. Available studies indicate that dietary insect inclusion can promote beneficial shifts in gut microbial communities, including increased bacterial diversity, enrichment of short-chain fatty acid-producing taxa, and reductions in selected opportunistic pathogens. However, these responses are not uniform across experimental models and depend on factors including insect species, processing method, dietary inclusion level, host species, age, and physiological status. Rather than acting through isolated mechanisms, insect-derived bioactive compounds function as an integrated nutritional matrix that simultaneously influences microbial metabolism, epithelial signaling, and immune regulation. Future standardized and multi-omics studies will be essential to identify the principal bioactive compounds responsible for these physiological effects and to optimize insect-derived functional ingredients for precision animal nutrition and more sustainable livestock and aquaculture production.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1912310</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1912310</link>
        <title><![CDATA[Sampling matters: the interplay of physiological parameters and performance over 1, 2 and 3 km in well-trained male endurance runners and sprinters]]></title>
        <pubdate>2026-10-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yannick M. Sondermann</author><author>Oliver J. Quittmann</author><author>Simon Nolte</author><author>Marco Fuchs</author><author>Gabriel Gehlert</author><author>Tina Foitschik</author><author>Thomas Abel</author>
        <description><![CDATA[AimTo examine characteristics associated with running performance in heterogeneous and endurance-only samples of well-trained male runners.MethodsTwenty well-trained (V̇O2max: 65.7 ± 5.5 ml·min-1·kg-1) male endurance runners (n=16) and sprinters (n=4), completed comprehensive laboratory testing and 100-m sprint as well as, 1-, 2-, and 3-km time-trials. Physiological markers included fractional utilization at maximal lactate steady-state (%V̇O2max), maximal fat oxidation rate (MFO), maximal lactate accumulation rate (ċLamax) and peak post-exercise lactate following the ramp test (LaRT). Hierarchical regression and bivariate correlations with Benjamini-Hochberg correction were used to examine performance associations and the influence of excluding sprinters.ResultsBaseline models (V̇O2max + running economy) explained <40% of 1000-m and >60% in 2000- and 3000-m performance in the pooled sample. MFO increased explained variance by 15.4% at 2000 m and +14.81% at 3000 m, while %V̇O2max added 11.3% at 3000 m. In the pooled sample, oxidative characteristics became more strongly associated with performance as distance increased, whereas several non-oxidative characteristics were positively associated with sprint performance and negatively associated with longer-distance performance. After excluding sprinters, associations of V̇O2max and MFO with 2000- and 3000-m performance were retained, whereas associations involving ċLamax and LaRT were attenuated. ASR remained negatively associated with 3000-m performance in both samples.ConclusionIn well-trained male runners, associations between physiological characteristics and running performance depend on event distance and sample composition. Oxidative characteristics were particularly relevant to 2000- and 3000-m performance, whereas the apparent relevance of several non-oxidative characteristics partly reflected the inclusion of sprinters. These sampling-related findings require confirmation in larger, balanced cohorts.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1912035</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1912035</link>
        <title><![CDATA[Predictive frameworks for youth basketball: a leakage-aware reassessment of athlete development and injury-risk models]]></title>
        <pubdate>2026-10-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Chen Yao</author>
        <description><![CDATA[IntroductionArtificial intelligence is increasingly applied in sports analytics; however, exceptionally high predictive performance may result from target construction, data leakage, or deterministic label structures. This study reassessed predictive models for youth basketball using a leakage-aware framework.MethodsA publicly available youth-basketball dataset containing 1,000 records and 25 variables was analyzed. Development-score construction and injury-risk label structure were audited. Construction-related predictors were subsequently excluded, and model performance was evaluated using repeated cross-validation and a locked 200-athlete holdout. Subgroup analyses by gender and age and an external-validation feasibility assessment were also conducted.ResultsDevelopment_Score was reconstructed almost perfectly from its documented components, with repeated cross-validation R2 of 0.999925. Injury_Risk_Level also demonstrated deterministic structure based on strength and endurance. After excluding construction-related predictors, locked-holdout performance decreased to 0.750 accuracy, 0.329 balanced accuracy, 0.286 macro-F1, and 0.622 macro AUC. High-risk sensitivity was 0.000 across the overall sample and examined subgroups. No compatible public dataset was identified for external validation.DiscussionThe initially exceptional performance largely reflected target construction and deterministic labeling rather than independent predictive information. These findings emphasize leakage-aware validation, transparent reporting, and cautious interpretation of sports-analytics prediction models.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1943433</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1943433</link>
        <title><![CDATA[Branched-chain amino acids in skeletal and cardiac muscles: a review of metabolic variations and cancer’s impact]]></title>
        <pubdate>2026-10-22T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Julian Chrzanowski</author><author>Wojciech Graboń</author><author>Karolina Buchajska</author><author>Agnieszka Cudnoch-Jędrzejewska</author>
        <description><![CDATA[Branched-chain amino acids (BCAA) - leucine, isoleucine, and valine - serve as essential regulators of energy homeostasis, protein turnover, and nutrient signaling in striated muscle. However, their metabolic processing varies substantially across tissues. This review contrasts BCAA metabolism in skeletal versus cardiac muscle and evaluates how cancer alters it. Skeletal muscle functions as the main site for whole-body BCAA transamination and oxidation, distributing these amino acids between protein synthesis and oxidative catabolism in line with physiological needs. In comparison, the myocardium maintains low baseline BCAA oxidation, depends primarily on fatty acids and glucose, and tightly limits BCAA catabolic flux to prevent the buildup of intermediates that would undermine mitochondrial function. In malignancies, BCAA metabolism is reconfigured in a way that depends on tumor type: many tumors increase BCAA uptake and suppress catabolism in order to preserve intracellular stores, as a result maintaining mechanistic target of rapamycin complex 1 (mTORC1) signaling and supporting proliferation. Using lung, pancreatic and colorectal cancers as main examples, we outline how this tumor-driven metabolic rewiring is linked to cancer cachexia - a multi-organ syndrome in which inflammation, mitochondrial dysfunction, and impaired anabolic signaling promote muscle and cardiac wasting rather than simple substrate limitation. We describe first the mechanisms shared by skeletal and cardiac muscle, then the features specific to each tumor type, and we distinguish throughout between cardiac evidence obtained in tumor-bearing hosts and inferences extrapolated from heart failure. We conclude that interventions directed at BCAA are most reasonable early in the disease course, and only when paired with approaches that suppress inflammation and restore mitochondrial quality control. We also identify priorities for tissue-specific biomarkers and for future research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1954055</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1954055</link>
        <title><![CDATA[Placebo-arm response rates for pain outcomes in chronic pancreatitis: a systematic review and meta-analysis of randomized controlled trials]]></title>
        <pubdate>2026-10-22T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Tareq Alsaleh</author><author>Prachi Mann</author><author>Aleena Majeed</author><author>Syed Hasaan Rahman</author><author>John George</author>
        <description><![CDATA[BackgroundImprovement in the placebo arm can influence chronic pancreatitis (CP) pain trials, yet contemporary estimates of placebo-arm response are limited. We aimed to quantify placebo-arm pain response rates in medical placebo-controlled randomized controlled trials (RCTs) of CP-related abdominal pain.MethodsPubMed, Web of Science, Embase, and Scopus were searched from inception to October 2025 for placebo-controlled RCTs reporting pain response among placebo-treated patients with CP. Crossover trials, procedural or device-based sham-controlled trials, and studies without extractable placebo-arm pain-response data were excluded. The primary outcome was the pooled proportion of placebo-treated patients achieving pain response according to study-specific definitions. Random-effects meta-analysis of single proportions was performed. Subgroup analyses categorized endpoints as partial pain improvement or complete pain resolution. Risk of bias was assessed using Cochrane RoB 2.ResultsSeven RCTs including 321 placebo-treated patients, 320 of whom contributed pain-response data, met inclusion criteria. Follow-up ranged from 3 to 26 weeks. One study was judged low risk of bias and six had some concerns; no study was high risk. The pooled placebo-arm pain response rate was 26% (95% CI, 17%–36%), with heterogeneity (I² = 74.8%). Response rates varied with endpoint stringency, although the difference between subgroups was not statistically significant (P = 0.18): 31% (95% CI, 18%–46%; I² = 73.7%) in trials using partial pain improvement criteria and 20% (95% CI, 12%–29%; I² = 42.1%) in trials requiring complete pain resolution. Leave-one-out sensitivity analysis did not materially alter the estimate.ConclusionsOne-quarter of placebo-treated patients in CP RCTs experience pain response. Endpoint stringency may influence observed placebo-arm response and should be considered in sample-size estimation, outcome selection, and interpretation of CP pain trials.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1953636</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1953636</link>
        <title><![CDATA[Structured effects of exercise on circulating brain-derived neurotrophic factor (BDNF) in postmenopausal women: a meta-analysis]]></title>
        <pubdate>2026-10-22T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Ying Zhou</author><author>Jianhui Chai</author><author>Jin Wang</author><author>Jian Wang</author>
        <description><![CDATA[ObjectiveTo systematically evaluate the effect of structured exercise interventions on circulating brain-derived neurotrophic factor (BDNF) levels among postmenopausal women, and to clarify the moderating effects of intervention modality, population characteristics, training duration, exercise intensity and energy-supply pattern on intervention outcomes, so as to provide evidence-based references for precise exercise interventions targeting brain health in postmenopausal women.MethodsFollowing the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement, electronic databases including PubMed, Web of Science, EBSCO and CNKI were searched for original studies regarding the effects of various exercise interventions on BDNF in postmenopausal women, from database inception to August 1, 2026. The Cochrane Risk-of-Bias Tool was applied for randomized studies. For quasi-randomized and non-randomized intervention studies, we explicitly acknowledge limitations of this tool and interpret methodological assessments cautiously; studies with insufficient randomization reporting were rated as unclear risk of bias. Meta-analysis was performed using Review Manager 5.4 software. Effect sizes were presented as standardized mean difference (SMD) with 95% confidence interval (95% CI). Subgroup analysis, sensitivity analysis and publication-bias evaluation were also conducted.ResultsTwelve studies involving 351 participants were finally included, with 173 subjects in the intervention group and 178 subjects in the control group. All included trials adopted chronic long-term structured exercise interventions without acute single-bout exercise protocols. Pooled meta-analysis demonstrated that structured exercise interventions significantly elevated BDNF levels in postmenopausal women compared with control conditions [SMD = 0.64, 95% CI (0.11, 1.17), P = 0.02], with substantial between-study heterogeneity (I² = 81%, P < 0.0001). Subgroup analyses (only subgroups with ≥3 studies included for quantitative synthesis) indicated that intervention modality, population characteristics, training duration and energy-supply pattern were potential main sources of heterogeneity. Statistically-significant maximum effect sizes were observed in the resistance training subgroup [SMD = 1.07, 95% CI (0.12, 2.01), P = 0.03], healthy older/postmenopausal-women subgroup [SMD = 0.30, 95% CI (-0.05, 0.65), P = 0.009], anaerobic-energy-supply-predominant subgroup [SMD = 1.07, 95% CI (0.12, 2.01), P = 0.03]. Some potential moderators could not be quantitatively evaluated because corresponding subgroups contained fewer than three primary studies, and those comparisons are only discussed as exploratory clues rather than robust conclusions. Sensitivity analysis revealed no substantial shift in pooled effect direction after sequential exclusion of individual studies. Funnel-plot inspection and Egger’s test detected no statistical evidence of publication asymmetry; nevertheless, these assessments were limited by the small number of included studies and cannot rule out publication bias definitively.ConclusionStructured exercise interventions can significantly increase peripheral BDNF levels in postmenopausal women, which suggests beneficial impacts on neuroplasticity and brain health for this population. Chronic resistance-based exercise regimens dominated by anaerobic energy-supply exert superior regulatory effects among healthy postmenopausal women.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420261468069, identifier CRD420261468069.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1975785</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1975785</link>
        <title><![CDATA[Mechanisms and targeted intervention strategies of macrophage mitochondrial quality control imbalance in the progression of atherosclerosis]]></title>
        <pubdate>2026-10-22T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Guo Zhili</author><author>Zhu Xiaoyu</author>
        <description><![CDATA[Atherosclerosis (AS) is a vascular disease characterized by lipid accumulation, chronic inflammation, and plaque instability, which can lead to severe cardiovascular events, such as myocardial infarction and stroke. Macrophages are the predominant immune cells within plaques and form foam cells upon uptake of oxidized low-density lipoprotein, a critical driver of AS progression. Recent studies have confirmed that imbalance of the mitochondrial quality control (MQC) system participates in the initiation and progression of AS; however, the imbalance in macrophage MQC as an upstream regulatory mechanism has not yet been systematically elucidated. MQC encompasses mitophagy, fusion-fission balance, mitochondrial biogenesis, and mitochondrial DNA (mtDNA) homeostasis. This imbalance can result in impaired clearance of damaged mitochondria, dysfunction of the electron transport chain, and excessive production of reactive oxygen species (ROS), which in turn activate the NLRP3 inflammasome and trigger inflammation and apoptosis. Concurrently, mitochondrial metabolic reprogramming can promote macrophage polarization toward the pro-inflammatory M1 phenotype while suppressing the anti-inflammatory M2 phenotype, thereby exacerbating lipid deposition and inflammatory amplification. Plaque macrophages are, however, heterogeneous: TREM2-high foamy macrophages are typically less inflammatory and metabolically distinct from adjacent non-foamy macrophages, cautioning against a purely linear glycolysis-M1-foam-cell sequence. Current research predominantly focuses on MQC imbalance, whereas a systematic integration of how imbalances in the MQC network mediate macrophage inflammation, foam cell formation, and plaque progression remains lacking. Intervention strategies targeting mitophagy activation, restoration of mitochondrial fusion-fission homeostasis, mitochondrial antioxidant defense, and macrophage-targeted delivery have demonstrated potential for alleviating plaque burden and stabilizing vulnerable plaques in preclinical studies. This review systematically summarizes the role and molecular mechanisms of macrophage MQC imbalance in AS, outlines existing controversies, research gaps, and novel targeted intervention strategies, and provides a theoretical basis for the development of new therapeutic targets for AS prevention and treatment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1922656</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1922656</link>
        <title><![CDATA[Dynamic machine learning architecture integrating time-phased predictions for acute kidney injury following extracorporeal membrane oxygenation]]></title>
        <pubdate>2026-10-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jianhai Lu</author><author>Zhen Chen</author><author>Donghua Zheng</author><author>Genglong Liu</author><author>Yijia Wu</author><author>Wanfang Li</author><author>Liuer Zuo</author><author>Qiang Tai</author>
        <description><![CDATA[BackgroundAcute kidney injury (AKI) is a frequent, severe complication of extracorporeal membrane oxygenation (ECMO) therapy, substantially contributing to unfavorable outcomes. No effective machine learning (ML) models exist for early, accurate detection. This study developed a two-phased prediction model using clinical data from pre-ECMO and on-ECMO stages for ECMO-induced AKI (ECMO-AKI), and further integrated two models to formulate a consensus risk-stratification strategy.MethodsThis retrospective study included 344 patients undergoing ECMO from 2015 to 2026. Clinical and laboratory variables from pre-ECMO and on-ECMO stages were respectively used to develop two ECMO-AKI diagnostic models via a analytical framework incorporating 12 ML algorithms. Multiple analytical methods were utilised to evaluate pre-ECMOAKI and on-ECMOAKI models. The Shapley Additive Explanations (SHAP) method was used to interpret two models and to quantify and visualize the features. Latent class growth mixture model (LCGMM) was applied to investigate the association between longitudinal feature trajectories and ECMO-AKI.ResultsPre-ECMOAKI and on-ECMOAKI models incorporated into 12 ML, yielding 66 and 91 combinations, respectively. Among these, glmBoost + gradient boosting machine (GBM) as a superior algorithm for predicting ECMO-AKI. Pre-ECMOAKI (9 features) and on-ECMOAKI (10 features) models exhibited superior discrimination performance, with area under curve (AUC) of 0.867 (95%CI: 0.819-0.911) and 0.907 (95%CI: 0.870-0.941) in derivation cohort, 0.732 (95%CI: 0.678-0.780) and 0.803 (95%CI: 0.711-0.889) in held-out validation cohort, respectively. A risk-stratification framework integrating pre-ECMOAKI and on-ECMOAKI predictions achieved a class-specific precision of 90.23% for ECMO-AKI events in the consensus high-risk group and 90.79% for non-ECMO-AKI events in the consensus low-risk populations. SHAP analysis reveals that endothelial activation and stress index (EASIX), cardiopulmonary resuscitation time (CPRT) and total bilirubin (TBI) are important feature variables in two models. Restricted cubic spline (RCS) regression, threshold effect analysis, and LCGMM indicated EASIX > 4.7 (with sustained increasing trend), CRPT > 24 min, and TBI > 20.2 μmol/L (with continuous upward trend) were associated with an elevated ECMO-AKI risk.ConclusionTwo-phased dynamic prediction models (pre-ECMOAKI and on-ECMOAKI) were constructed based on glmBoost +GBM, which act as an accurate and interpretable diagnostic tool for ECMO-AKI. Based on consistency analysis of predictions of two models, this framework allows early risk stratification and thus holds potential for individualized management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1974885</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1974885</link>
        <title><![CDATA[Brain–heart coupling in Parkinson’s disease: from autonomic dysfunction to network physiology]]></title>
        <pubdate>2026-10-22T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Pasquale Pagliaro</author>
        <description><![CDATA[Cardiovascular autonomic dysfunction is a well-established feature of Parkinson’s disease (PD), yet the brain and cardiovascular system are still largely investigated as separate physiological domains. This separation may overlook an important dimension of PD pathophysiology: the dynamic communication between them. Here, we examine emerging evidence that brain–heart coupling itself is altered in PD. A focused PubMed search identified studies directly relating neural activity to cardiac dynamics, complemented by relevant physiological and autonomic literature. Despite a small and heterogeneous evidence base, electrophysiological, neuroimaging, and dynamic network studies suggest disrupted central–cardiac coordination. Alterations are detectable in early and de novo PD, relate to dysautonomia, and appear sensitive to dopaminergic state. Emerging evidence for impaired cardiac interoception further suggests that dysfunction may extend from descending autonomic control to ascending heart-to-brain processing. Importantly, cross-system measures can reveal abnormalities that remain not captured by neural or cardiovascular signals alone. Their clinical potential is promising but remains to be established through larger, standardized, and longitudinal studies. At present, brain–heart coupling is best viewed as a physiological framework with emerging translational relevance rather than as a validated biomarker. By revealing interactions that remain hidden when neural and cardiovascular systems are examined separately, brain–heart coupling may uncover a distinct dimension of PD pathophysiology and provide a bridge from integrative physiology to disease phenotyping and future clinical stratification.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1961052</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1961052</link>
        <title><![CDATA[Application of radial artery signal characteristics in long-term head-down bed rest experimental cardiovascular status assessment]]></title>
        <pubdate>2026-10-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kaiting Ha</author><author>Xiaojuan Hu</author><author>Dong Liu</author><author>Guohao Zhang</author><author>Shuyi Zhang</author><author>Shiju Zhao</author><author>Liping Tu</author><author>Tao Jiang</author><author>Xuxiang Ma</author><author>Quanchun Fan</author><author>Junlian Liu</author><author>Chengpu Zhang</author><author>Hongzhi Shi</author><author>Jiatuo Xu</author><author>Ji Cui</author>
        <description><![CDATA[ObjectiveThis study aims to observe pulse graph parameters and their dynamic changes in subjects of the head-down bed rest (HDBR) under different exercise interventions and to evaluate their application value in simulating cardiovascular function changes in weightlessness.MethodsA total of 36 male volunteers (32.0 ± 2.6 years) participated in a 138-day experiment (15 days at baseline, 90 days at -6° HDBR, and 33 days at recovery). Radial pulse graphs were collected at 11 time points: the baseline, D7, D15, D30, D45, D60, D75, D90 during bedrest, and R + 7, R + 15, and R + 30 during the recovery. Cardiac structural and functional parameters, along with arterial elasticity and blood flow parameters, were recorded simultaneously. The feasibility of TCM pulse diagnosis for assessing cardiovascular status in HDBR subjects was explored through correlation analyses between pulse parameters and ultrasound indicators.Results(1) During bedrest, pulse parameters h1, h3, h4, t5, t, As, Ad, and h4/h1 showed an upward trend and decreased during the recovery stage. PWVρ, crPWV, LICAvmax, and LFAvmax increased initially and then decreased, whereas IMT showed a sustained increase. (2) The aerobic exercise plus resistance training group showed faster adaption to HDBR and better cardiovascular functional recovery after long-term HDBR. (3) Canonical correlation and bivariate correlation analyses showed varying degrees of correlation between the two types of indicators, with some correlation coefficients >0.7 (P < 0.05). (4) Repeated measurements showed statistically significant differences in pulse graph parameters, with cfPWV, crPWV, and PWVρ showing an increasing trend followed by a decrease.ConclusionCardiovascular changes induced by HDBR can be reflected in pulse graph parameters; radial pulse wave parameters may serve as valuable references for the dynamic monitoring and assessment of cardiovascular function under simulated weightlessness.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1892963</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1892963</link>
        <title><![CDATA[Rehabilitation efficacy of neuromuscular training for individuals suffering from knee osteoarthritis: a systematic review and meta-analysis based on randomized controlled trials]]></title>
        <pubdate>2026-10-21T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Bihui Bai</author><author>YuBiao Gu</author><author>Li Dingpeng</author><author>Xingwen Xie</author><author>Fei Yao</author>
        <description><![CDATA[ObjectiveThis study aimed to comprehensively assess the efficacy of neuromuscular training (NMT) in function, symptoms, quality of life (QoL), pain, and safety in individuals with knee osteoarthritis (KOA), thereby providing evidence-based support for rehabilitation strategies in KOA management.MethodsThis study was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We systematically searched PubMed, Embase, Web of Science, and the Cochrane Library from database inception to August 30, 2025. Randomized controlled trials (RCTs) assessing NMT for KOA were included. For multiple reports originating from the same underlying randomized trial, a trial family was established based on trial registration number, randomized sample size, baseline characteristics, intervention protocols, and follow-up duration to avoid duplicate counting. A random-effects model was applied for meta-analysis, and sensitivity analysis, publication bias assessment, prespecified subgroup analyses, and tests for subgroup interactions were performed. The certainty of evidence for primary outcomes and adverse events was evaluated using the approach proposed by the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) Working Group.ResultsA total of 17 study reports were included, corresponding to 14 independent RCTs with 1,029 participants, of whom 516 were in the NMT group and 513 in the control group. Compared with control interventions, NMT significantly alleviated KOOS Symptoms (MD = 4.44, 95% CI: 1.62, 7.26, P = 0.002), KOOS ADLs (MD = 3.94, 95% CI: 0.09, 7.79, P = 0.04), and KOOS QoL (MD = 5.59, 95% CI: 0.97, 10.21, P = 0.02). The between-group differences for KOOS Pain (MD = 1.95, 95% CI: -0.27, 4.17, P = 0.08) and KOOS Sport/Rec (MD = 1.64, 95% CI -2.24, 5.53, P = 0.41) did not reach statistical significance. The meta-analysis of adverse events showed no statistically significant difference in the incidence of adverse events between the NMT and control groups (RR = 0.83, 95% CI: 0.50, 1.37, P = 0.46). Nevertheless, given the heterogeneity across studies in the definitions, monitoring, and reporting of adverse events, this result should not be interpreted as evidence of equivalent safety between the interventions. The subgroup analyses suggested differences in certain specific subgroups. Most subgroup interaction tests were not statistically significant; however, a significant interaction was observed for mean age in the KOOS QoL analysis (P for interaction = 0.02), which should be interpreted cautiously given the limited number of studies.ConclusionNMT may partially alleviate comprehensive symptoms, facilitate activities of daily living, and enhance knee-related QoL in patients with KOA, whereas consistent benefits were not demonstrated for KOOS Pain, sport and recreational function, or most objective functional outcomes. No statistically significant difference in reported adverse events was observed; however, heterogeneity in adverse-event definitions and reporting limits conclusions regarding comparative safety. Additional well-designed RCTs with standardized NMT protocols, adequate sample sizes, and longer follow-up are needed to confirm the magnitude and clinical relevance of these effects.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420251118258, identifier CRD420251118258.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1922514</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1922514</link>
        <title><![CDATA[CRP-derived lower-limb coordination pattern distributions and frequency-band trunk–lower limb intermuscular coherence during badminton backhand footwork: a cross-sectional study]]></title>
        <pubdate>2026-10-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hongbing Xie</author><author>Hangyuan Li</author>
        <description><![CDATA[ObjectiveTo compare complete-cycle lower-limb coordination-pattern distributions and frequency-band-specific trunk–lower limb intermuscular coherence during a standardized badminton backhand footwork–backhand-clear task between elite and amateur players.MethodsThirty-six male badminton players were classified into elite and amateur groups (n=18 each). Each participant completed 10 valid trials. Three-dimensional kinematics and surface electromyography were synchronously recorded using Qualisys and Delsys Trigno systems. Continuous relative phase waveforms were summarized as four coordination-pattern percentages for the hip–knee, hip–ankle, and knee–ankle pairs. Intermuscular coherence was quantified as the area of significant coherence (AZ) for 21 trunk–lower limb muscle pairs across α, β, and γ bands. Trial-level linear mixed-effects models included group, trial, and their interaction as fixed effects and participant as a random intercept. Years of badminton training were not included as a covariate, as the objective was to compare competitive-level groups within their existing training backgrounds. Benjamini–Hochberg false discovery rate (FDR) correction was applied separately to 12 coordination and 63 coherence comparisons.ResultsAfter FDR correction, elite players showed higher hip–knee in-phase and lower anti-phase proportions, higher proximal-dominant and lower distal-dominant proportions for hip–ankle and knee–ankle coordination, and a higher knee–ankle anti-phase proportion (all q=0.025). Although 23 coherence comparisons had raw P<0.05, none survived FDR correction (all q≥0.098).ConclusionElite and amateur players differed in selected complete-cycle coordination-pattern distributions, with greater proximal contribution to hip–ankle and knee–ankle coordination in elite players. No muscle-pair–frequency-band coherence difference remained significant after FDR correction. These task-specific, cross-sectional findings do not identify the timing of coordination differences, establish causal effects of training, or demonstrate competitive-level associations independent of training duration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1963705</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1963705</link>
        <title><![CDATA[Pericyte-mediated intercellular crosstalk in renal fibrosis: regulatory mechanisms and intervention strategies]]></title>
        <pubdate>2026-10-21T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Lei Tang</author><author>Wei Qiao</author><author>Suyu Wang</author><author>Zhao Wang</author><author>Shaohong Zhang</author><author>Ling Liu</author><author>Wenbo Zhu</author>
        <description><![CDATA[Chronic kidney disease continues to increase in global prevalence, with renal fibrosis serving as a major pathological driver of end-stage renal disease and imposing a substantial burden on global public health. Renal pericytes, essential mesenchymal cells distributed along capillary walls, have been redefined from mere structural vascular support cells to multidirectional communication hubs that coordinate homeostasis of the renal microenvironment. Under persistent injurious stimuli, pericytes detach from capillary walls, migrate, and become activated, undergoing pericyte-to-myofibroblast transition and emerging as a predominant source of renal interstitial myofibroblasts. This process promotes capillary rarefaction and aberrant extracellular matrix deposition, thereby establishing a vicious cycle of “vascular loss–exacerbated hypoxia–progressive fibrosis”. Herein, the pericyte-mediated cellular interactome and its molecular regulatory mechanisms in renal fibrosis are systematically reviewed, with particular emphasis on the bidirectional communication of pericytes with vascular endothelial cells, renal tubular epithelial cells, immune cells (including macrophages, T lymphocytes, neutrophils, and mast cells), and fibroblasts; direct renal evidence for these interactions is explicitly distinguished from indirect or hypothetical mechanisms inferred from non-renal models. The roles of key signaling pathways, including Ang/Tie2, PDGF/PDGFRβ, TGF-β/Smad, Hippo-YAP/TAZ, Wnt/β-catenin, and Notch, in regulating these interactions are further elucidated, with clarification of the extent to which each pathway is pericyte-intrinsic or involves pericytes as one of several effector cell types. Additionally, recent advances in intervention strategies targeting pericyte-mediated crosstalk are critically appraised according to the directness of pericyte targeting and the strength of the supporting evidence, encompassing mesenchymal stem cell therapy, engineered extracellular vesicles, nanomedicine-based drug delivery systems, and natural pharmaceutical therapies. Current evidence remains constrained by the lack of pericyte-specific markers, the reliance on rodent models, and the predominantly preclinical stage of available interventions; nevertheless, a comprehensive understanding of the pericyte-mediated cellular interactome may provide an important theoretical foundation and candidate therapeutic targets for the prevention and treatment of renal fibrosis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1973245</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1973245</link>
        <title><![CDATA[Effects of movement initiation pattern on dynamic postural stability across two individualized drop heights during single-leg landing in young men]]></title>
        <pubdate>2026-10-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ying Li</author><author>Ruiqi Cheng</author><author>Idsart Kingma</author><author>Chris Bishop</author><author>Weijie Fu</author><author>Fei Li</author><author>Ming Li</author><author>Christophe Hautier</author><author>Qingshan Zhang</author>
        <description><![CDATA[ObjectivesSingle-leg landing protocols differ in task components. We estimated pattern differences in vertical time to stabilization (V-TTS) and the Dynamic Postural Stability Index (DPSI) at two individualized heights, with 95% confidence intervals, and tested whether they changed with height.MethodsIn a within-participant 3 × 2 factorial experiment, twenty-three healthy young male strength and conditioning students (5.7 ± 3.2 years of systematic sports training) completed randomized step-off (SOL), single-leg jump (SLJL), and single-leg hop (SLHL) landings at two individualized drop heights derived from countermovement jumps. Linear mixed-effects models tested pattern, height, and interaction effects on TTS and DPSI; statistical parametric mapping compared take-off and landing force waveforms.ResultsPattern × Height interactions occurred for V-TTS (p = 0.004) and DPSI (p = 0.001). At Low, the largest contrasts were SLHL-SOL for V-TTS (0.15 s; 95% CI, 0.11 to 0.20) and DPSI (0.079; 95% CI, 0.066 to 0.092; adjusted p < 0.001 for both). At High, both active patterns differed from SOL (V-TTS, 0.06-0.07 s; DPSI, 0.041-0.054; adjusted p ≤ 0.014) with no clear difference between the active patterns after adjustment. The SLHL–SOL and SLHL–SLJL differences for V-TTS and the SLJL–SOL and SLHL–SOL differences for DPSI were larger at Low, whereas the V-TTS SLJL–SOL and DPSI SLHL–SLJL contrasts showed no clear change. Horizontal TTS showed no adjusted differences. Take-off and landing interactions involved all force components.ConclusionsIn healthy young men, movement initiation pattern altered V-TTS and DPSI at both heights, and some differences varied with height. Cross-study comparisons should match initiation pattern and prescribed height.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1982421</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1982421</link>
        <title><![CDATA[Topological transition at midlife in the physiological network of Mexican women and divergent amplitude of topological change between sexes: allostatic load biomarkers across adult life]]></title>
        <pubdate>2026-10-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Julian B. Uriarte-Ortiz</author><author>Antonio Barajas-Martínez</author><author>Ruth M. López-Mayorga</author><author>Raúl Sampieri-Cabrera</author>
        <description><![CDATA[IntroductionAdditive allostatic load indices treat cardiometabolic biomarkers as independent Q6 units and discard their covariation. Correlation networks recover it, yet previous physiological network studies were restricted to strictly healthy participants or specific diseases, leaving undescribed how topology changes across adult life in the general population.MethodsWe analyzed 7,999 adults (5,058 women, 2,941 men) pooled from the Mexican National Health and Nutrition Surveys (ENSANUT) of 2016, 2020 and 2021, stratified by sex and five age groups (20–91 years) and, in an exploratory analysis, by dyslipidemia. For each stratum we built graphs of 22 anthropometric, hemodynamic and biochemical variables from Spearman correlations retained at p < 0.05 and averaged density, transitivity, mean distance and Louvain modularity over 100 subsamples of 79% of the participants.ResultsFemale topology followed two phases. Between the 20–29 and 40–49 age groups, density fell from 0.47 to 0.25 and transitivity from 0.70 to 0.50, whereas mean distance rose from 1.61 to 2.32 and modularity from 0.40 to 0.56 as blood pressure variables separated into a distinct module; all four then plateaued through the oldest group. Univariate biomarker trajectories changed gradually over the same ages. Men showed no such transition, with density between 0.34 and 0.42 across all strata, a range narrower than each female step during the first phase, and modularity rising only from 0.37 to 0.45 between the two youngest groups. The female decline was already present between the 20–29 and 30–39 groups, at ages preceding the menopausal transition. Edges persisted in graphs rebuilt from the 12 directly measured variables, and stratification by dyslipidemia, defined by three nodes of the network, did not fully account for the age trends.DiscussionThese cross-sectional graphs describe covariation across individuals, and their reading as within-person regulation requires longitudinal confirmation. A male transition before age 20 and survivorship selection remain competing, testable explanations for male topological stability. The results extend to adult life the sexual dimorphism described in physiological networks of healthy young adults and locate in women a reorganization, completed by midlife, that univariate analyses did not reveal.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1940305</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1940305</link>
        <title><![CDATA[Regulation of gastrin-releasing peptide gene expression in chickens]]></title>
        <pubdate>2026-10-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kefan Tang</author><author>Xuan Tian</author><author>Xiaohan Yuan</author><author>Yanrong Li</author><author>Jiannan Zhang</author><author>Yajun Wang</author><author>Juan Li</author>
        <description><![CDATA[Gastrin-releasing peptide (GRP) is a neuropeptide with diverse physiological functions in mammals. Similar to its mammalian counterparts, chicken GRP (cGRP) is expressed in endocrine cells of the gastrointestinal tract, including the proventriculus, where it regulates gastric acid secretion. Our previous study showed that cGRP is predominantly expressed in the anterior pituitary and acts as a novel pituitary hormone that promotes the survival of small ovarian follicles. Using primary pituitary cell cultures, we found that gonadotropin-releasing hormone 1 (GnRH1) markedly increased cGRP mRNA abundance in both dose- and time-dependent manners. Pharmacological analyses suggested that this effect likely involved the AC/cAMP/PKA pathway and the PLC/PKC/MEK/ERK pathway. We also examined the regulation of GRP expression by sex steroids. 5α-dihydrotestosterone (DHT) and progesterone (P4) downregulated GRP expression in cultured chicken pituitary cells, whereas 17β-estradiol (E2) upregulated GRP expression in dose- and time-dependent manners. Analysis of the isolated GRP 5′-flanking region identified potential estrogen receptor-binding sites, providing a molecular basis for E2-mediated upregulation of GRP expression. These findings support cGRP as a novel pituitary hormone under hypothalamic GnRH1 control and feedback regulation by sex steroids. Together with its reported role in the survival of small ovarian follicles, cGRP may contribute to the regulation of egg production in chickens.]]></description>
      </item>
      </channel>
    </rss>