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        <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>2026-05-05T05:18:55.698+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1757655</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1757655</link>
        <title><![CDATA[Interaction analysis of tight junction proteins by Förster resonance energy transfer is recommended in live cells rather than after paraformaldehyde fixation]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Catrin Przibylla-Diop</author><author>Marianne Musinszki</author><author>Markus Bleich</author><author>Susanne Milatz</author>
        <description><![CDATA[The tight junction regulates the paracellular passage of solutes and water. It is primarily constituted by the family of claudins which assemble to huge multimers and basically seal the paracellular cleft. Certain claudins, however, can function as subunits of selective paracellular channels and thereby mediate paracellular ion and water flux across epithelia. In the thick ascending limb of Henle’s loop (TAL), ion handling depends on the spatial separation of paracellular sodium and magnesium transport. Magnesium is conducted via a claudin-16/19 complex, whereas sodium permeation is enabled by claudin-10b which forms autonomous tight junctions without interacting with other TAL claudins. Förster resonance energy transfer (FRET) analysis is a well-established technique to study protein-protein interactions, based on the non-radiative energy transfer between closely positioned donor and acceptor chromophores. FRET has been broadly used to analyze claudin oligomerization as a prerequisite for tight junction formation. Although FRET can be performed in both living and fixed cells, comparability between these conditions remains poorly characterized. While fixed-cell FRET analyses are common for transmembrane ion channels, data for claudins under fixation are lacking. In this study, we evaluated the suitability of paraformaldehyde fixation for analyzing interaction between TAL claudins -10b and -19. Using acceptor photobleaching FRET, we compared the energy transfer efficiencies in live and fixed cells expressing fluorophore-tagged claudins. Fixation markedly altered energy transfer efficiency, leading to false-positive evaluation of apparent claudin interactions. These findings demonstrate that paraformaldehyde fixation compromises the accuracy of FRET measurements and indicate that FRET analyses are best performed in living cells.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1838823</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1838823</link>
        <title><![CDATA[Improvement of occipital neuralgia by pulsed radiofrequency of the greater occipital nerve combined with local magnesium sulfate injection: a randomized controlled study]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jialei Zhang</author><author>Zhishan Zhang</author><author>Enquan Song</author><author>Jie Wu</author>
        <description><![CDATA[ObjectiveTo investigate the safety and efficacy of magnesium sulfate as an adjuvant in pulsed radiofrequency (PRF) stimulation of the greater occipital nerve for the treatment of occipital neuralgia.MethodsConsecutive patients diagnosed with neurogenic occipital neuralgia who attended the Pain Department of Changzhi People’s Hospital were recruited for this study, randomly assigned to control group and experimental group. The control group received PRF treatment on the affected side only, whereas the experimental group received an additional perineural injection of 5% magnesium sulfate (150 mg) around the greater occipital nerve immediately after PRF. NRS scores, pain duration, and pain frequency were compared between the two groups at baseline (T0), 30 days post-treatment (T1), and 60 days post-treatment (T2), at these identical time points, ultrasonography was performed to measure the thicknesses of the ipsilateral semispinalis capitis, obliquus capitis inferior, and deep fascia superficial to the obliquus capitis inferior, along with vertebral artery systolic flow parameters. Additionally, shear wave elastography (SWE) was used to measure the maximum shear wave velocity (SWVmax) and mean shear wave velocity (SWVmean) of the semispinalis capitis to assess cervical musculature status.ResultsA total of 91 patients completed the entire study, with 43 in the control group and 48 in the experimental group. No significant between-group differences were observed preoperatively in occipital neuralgia symptoms (NRS scores, pain duration, and frequency), thickness of the ipsilateral perineural muscles and fascia, shear wave elastography of the semispinalis capitis, or vertebral artery hemodynamic parameters (P>0.05). Pain symptoms were significantly reduced after treatment compared with preoperative levels in both groups(P < 0.05), and patients in the experimental group exhibited significantly alleviated pain symptoms compared with the control group (P < 0.05). No significant differences were detected in muscle, fascia, or vertebral artery parameters in the control group between pre- and post-treatment assessments (P>0.05). In contrast, all parameters of muscle, fascia, and vertebral artery in the experimental group were significantly improved post-treatment compared with baseline (P < 0.05).ConclusionLocal magnesium-sulfate injection enhances pulsed radiofrequency efficacy by relieving perineural muscle spasm and improving vertebral-artery hemodynamics, leading to sustained reductions in headache intensity, duration, and frequency with an excellent safety profile.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1754745</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1754745</link>
        <title><![CDATA[Cutaneous lymphatics and skin diseases: mechanisms, imaging modalities, and future therapeutic strategies]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Nuoran Chen</author><author>Duoduo Gu</author><author>Wanqing Yang</author><author>Xiaoqi Meng</author><author>Tingwei Liu</author><author>Dansheng Li</author><author>Yang Xu</author>
        <description><![CDATA[Cutaneous lymphatic vessels are essential for maintaining tissue homeostasis and coordinating immune defence, making them vital to skin health. Recent advances in molecular biology and immunology have revealed the association between lymphatic dysfunction and various dermatological conditions, including skin aging, psoriasis, systemic lupus erythematosus, and cutaneous squamous cell carcinoma. Lymphatic structure and function alterations influence immune regulation and play active roles in inflammatory responses and tissue repair processes. This study provides a systematic review of the biological characteristics of cutaneous lymphatic vessels, their mechanistic contributions to disease pathogenesis, and current lymphatic imaging methodologies. Emerging therapeutic strategies targeting lymphatic regulation represent a promising direction for dermatological interventions, with prospects for future research and clinical translation. By elucidating the pathophysiological mechanisms underlying cutaneous lymphatic activity, the aim of this review was to provide novel theoretical foundations and strategic insights for the prevention and treatment of related diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1795836</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1795836</link>
        <title><![CDATA[Effects of chronic sleep deprivation on the bone mineral density, bone microarchitecture and body weight of mice: exploratory study]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Weiwei Xiang</author><author>Zhen Lv</author><author>Xinwen Min</author><author>Junhao Zhang</author><author>Handong Yang</author><author>Jun Chen</author><author>Jishun Chen</author><author>Dongfeng Li</author><author>Hao Xu</author><author>Chao Luo</author><author>Wenwen Wu</author>
        <description><![CDATA[ObjectiveThis study aimed to investigate the long-term effects of chronic sleep deprivation (CSD) on the bone mineral density (BMD), bone microarchitecture, biomechanical properties and body weight of middle-aged and older male C57BL/6 mice.MethodsTwenty-one 8-month-old mice were randomly assigned to a CSD group (n = 9) or a control group (n = 12). The CSD group was subjected to sleep deprivation using an automated sleep deprivation apparatus for 3 months. Trabecular bone microarchitecture at the distal femur was evaluated by microcomputed tomography. Femoral biomechanical properties were assessed using a three-point bending test, and body weight was monitored weekly throughout the experiment.ResultsThree months of CSD significantly reduced BMD, bone volume (BV) and trabecular thickness (Tb.Th) compared with those of the control group (all P < 0.05). Trabecular separation (Tb.Sp) and bone surface (BS) were also significantly decreased (P < 0.05). No significant differences were observed in trabecular number (Tb.N), bone volume fraction (BV/TV) or other microarchitectural parameters. Three-point bending test showed no statistically significant differences in any biomechanical indices, including maximum load, bending stiffness and elastic modulus (all P > 0.05), between the two groups. Body weight monitoring revealed that the CSD group had significantly lower body weight at the early stage of the experiment (week 1) and at week 8 compared with the controls (P < 0.05). No significant differences were observed at most other time points, showing a fluctuating pattern with baseline differences.ConclusionThree months of CSD led to decreased BMD and trabecular thinning in middle-aged and older male mice. No significant deterioration of overall bone biomechanical properties was observed, suggesting the presence of compensatory mechanisms in bone. The effect of sleep deprivation on body weight was intermittent rather than sustained. These findings provide experimental evidence for a comprehensive understanding of the relationship between sleep duration and skeletal health.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1837615</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1837615</link>
        <title><![CDATA[Effects of plyometric training on strength, explosive performance, and agility in female team-sport athletes: a systematic review and three-level meta-analysis]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Zhuo Zeng</author><author>Peng Zhang</author><author>Chengyu Zhou</author><author>Zixin Wang</author><author>Junhao Li</author><author>Qi Xie</author><author>Haoran Li</author><author>Dongxu Huang</author><author>Yongmin Xie</author><author>Aiguo Zhou</author>
        <description><![CDATA[IntroductionPlyometric training (PT) is widely used in team sports, but its outcome-specific effects in female team sport athletes and the influence of key programming variables remain unclear.MethodsThis systematic review and three-level meta-analysis examined the effects of PT on strength, jumping, sprinting, throwing, and agility in female team sport athletes and explored whether training frequency, intervention duration, and ground contacts per session moderated these effects. Randomized and non-randomized controlled trials were identified through database searches and manual screening. A three-level random-effects meta-analysis with cluster-robust variance estimation was performed. Subgroup analyses and meta-regressions examined potential moderators, and certainty of evidence was assessed using GRADE. Thirty-six studies involving 921 participants were included.ResultsPT significantly improved vertical jump (SMD = 0.67), horizontal jump (SMD = 0.70), sprint (SMD = -0.85), throwing (SMD = 0.91), and agility (SMD = -1.09). Effects on strength were inconsistent (p = 0.0025), with improvements in upper-body (SMD = 1.09) but not lower-body strength (SMD = 0.08). Competitive level moderated agility outcomes, whereas age was not a consistent moderator. Meta-regression showed no clear associations of training frequency, intervention duration, or ground contacts per session with performance changes. Certainty of evidence ranged from very low to moderate.Discussion/conclusionPT can be an effective training strategy for improving multiple outcomes in female team sport athletes, particularly jumping, sprinting, throwing, and agility. However, adaptations appear outcome-specific, and evidence is insufficient to identify programming variables that consistently influence outcomes. Further studies with larger and more diverse samples are needed.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420261328856, identifier CRD420261328856.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1773684</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1773684</link>
        <title><![CDATA[Perinatal vulnerability: its impact on oral and craniofacial hard tissue development]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Takehito Ono</author>
        <description><![CDATA[Advances in perinatal and neonatal medicine have dramatically improved the survival rates of infants with perinatal vulnerabilities of preterm birth (PTB), low birth weight (LBW) or small for gestational age (SGA), by rescuing these infants from immediate postnatal complications. Despite improved survival from such problems, it has in turn highlighted long-term complications, including psychiatric, neurological, respiratory, cardiovascular and metabolic diseases. In the oral and craniofacial regions, perinatal vulnerability is associated with an increased risk of developmental complications, including bone deformities, malocclusion and tooth malformations. These anomalies are often tangible and can be recognized earlier than extracranial sequelae; thus, they may serve as accessible indicators for predicting extracranial sequelae that remain latent. Oral and craniofacial sequelae are considered consequences of changes in nutritional status and oxygen saturation before and after birth, which are related to epigenetic changes. Additionally, the development of oral and craniofacial tissues is controlled by mechanical forces. The underlying mechanisms have not been fully elucidated, and future studies elucidating these mechanisms will enhance diagnostic and therapeutic strategies, as well as prognostic accuracy, ultimately improving long-term outcomes for infants born with perinatal vulnerabilities.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1809107</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1809107</link>
        <title><![CDATA[Taurine and glutamine supplementation in aging: systemic mechanisms, exercise interactions, and modulation of muscular and neurobiological pathways]]></title>
        <pubdate>2026-05-04T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Zhigang Chen</author><author>Zhiwei Niu</author>
        <description><![CDATA[The senescence of the neuro-skeletal muscle system is typified by a gradual deterioration in muscle mass, strength, neuromuscular efficacy, and cognitive capabilities, which is further exacerbated by metabolic dysregulation and heightened vulnerability to fatigue. The identification of efficacious strategies aimed at reversing or mitigating these deficits is paramount for the promotion of healthy aging. Taurine, glutamine, and physical exercise emerge as promising modulators of cellular homeostasis, exhibiting synergistic potential to address multiple pathways implicated in age-associated decline. This review amalgamates mechanistic insights into the effects of taurine and glutamine supplementation, in conjunction with exercise regimens, on protein metabolism, mitochondrial functionality, muscle fatigue biomarkers, neuroinflammation, redox equilibrium, and body composition throughout the aging process. We examine the role of taurine in preserving calcium homeostasis, enhancing mitochondrial stability, and mitigating oxidative stress; the function of glutamine in sustaining nitrogen balance, regulating immune responses, and facilitating energy metabolism; and the ability of exercise to stimulate critical signaling cascades and antioxidant networks. The integration of taurine and glutamine supplementation with systematically designed exercise regimens may yield a holistic, multi-faceted strategy for counteracting neuro–skeletal muscle aging and augmenting overall functional capacity in the elderly population.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1811001</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1811001</link>
        <title><![CDATA[Aldosterone increases the expression and subcellular localization of SERCA2a and SERCA2b in the rat mesenteric artery]]></title>
        <pubdate>2026-05-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Cristian J. Arriero-Carrillo</author><author>Hiram Lozano-Ruiz</author><author>Agustín Guerrero-Hernández</author><author>Federico Castro-Muñozledo</author><author>Angélica Rueda</author>
        <description><![CDATA[Aldosterone (Aldo), a mineralocorticoid hormone, modulates cardiovascular function by regulating the expression of intracellular Ca2+ handling proteins, among other effects. In rat resistance-sized mesenteric arteries (MA), Aldo treatment (10 nM, 24 h) upregulates both the L-type voltage-gated Ca2+ channel α1C subunit (CaV1.2) and the Sarco/Endoplasmic Reticulum Ca2+ ATPase (SERCA pump), thereby increasing Sarcoplasmic Reticulum (SR) Ca2+ load. Two SERCA isoforms, SERCA2a and SERCA2b, are expressed in rat MA, but their specific physiological contributions to distinct intracellular Ca2+ signals, remain unclear. In this study, we characterized the relative abundance and subcellular distribution of SERCA2a and SERCA2b in rat MA, their regulation by Aldo, and the impact of Aldo-induced SERCA remodeling on local Ca2+ signals relevant to vascular function, such as Ca2+ sparks and Ca2+ waves. Aldo-treated MA smooth muscle cells (MASMC) exhibited increased Ca2+ spark frequency and a higher incidence of spontaneous Ca2+ waves. Aldo augmented both protein and mRNA levels of SERCA2a and SERCA2b, effects that were blocked by the mineralocorticoid receptor (MR) antagonist RU28318. Under control conditions, SERCA2a was predominantly localized in the perinuclear region, whereas SERCA2b was distributed across both subplasmalemmal and perinuclear regions. Aldo treatment increased the expression of both isoforms in all analyzed subcellular compartments (subplasmalemmal, cytoplasmic, and perinuclear), with a pronounced redistribution towards the subplasmalemmal region of MASMC. This shift in SERCA subcellular distribution likely contributes to enhanced superficial Ca2+ buffering and the ignition of Ca2+ sparks and Ca2+ waves. Furthermore, Aldo increased mRNA levels of mitochondrial transcription factors A and B2 (TFAM and TFB2M), previously implicated in SERCA regulation in human aorta, suggesting a transcriptional mechanism whereby MR activation of the SERCA2 gene is associated with increased TFAM and TFB2M expression. Collectively, these findings demonstrate for the first time that Aldo increases the expression and promotes the subplasmalemmal localization of SERCA2a and SERCA2b in MASMC. This remodeling underscores their critical role in maintaining the superficial Ca2+ buffering system and SR Ca2+ load to prevent pathological elevations in the intracellular Ca2+ concentration. Our results highlight the SERCA pump as a potential therapeutic target in hypertension associated with hyperaldosteronism.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1716764</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1716764</link>
        <title><![CDATA[Direct dapagliflozin exposure enhances respiration and membrane hyperpolarization in isolated cardiac mitochondria]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Itanna Isis Araújo de Souza</author><author>César Francisco Maricato da Rosa</author><author>Laís Eduardo Marinho</author><author>Marcella Borges Coutinho</author><author>Caroline Da Silva Moraes</author><author>Antonio Carlos Campos de Carvalho</author><author>José Hamilton Matheus Nascimento</author><author>Leonardo Maciel de Oliveira Pinto</author>
        <description><![CDATA[Dapagliflozin, a sodium–glucose cotransporter 2 (SGLT2) inhibitor widely used for the treatment of diabetes, has been consistently associated with cardiovascular protection, including attenuation of ischemia/reperfusion injury and reduced incidence of heart failure. However, the cellular and molecular mechanisms underlying these effects remain incompletely understood. In this context, the present study aimed to investigate whether dapagliflozin exerts direct effects on mitochondrial function and bioenergetics. Cardiac mitochondria were isolated from Wistar rats (Rattus norvegicus), and mitochondrial function was systematically evaluated by assessing oxygen consumption, ATP production, reactive oxygen species (ROS) generation, and mitochondrial membrane potential following exposure to dapagliflozin (10 nM). Dapagliflozin increased oxygen consumption in states 1–3 supported by complex I substrates and enhanced both basal and ADP-stimulated respiration in complex II, without affecting state 4 respiration, complex IV activity, or maximal uncoupled respiration. In parallel, dapagliflozin significantly reduced mitochondrial ROS production in both complexes I and II without altering ATP generation, resulting in an increased ATP/ROS ratio, indicative of improved bioenergetic efficiency. Notably, electron leakage was increased in complex I but remained unchanged in complex II, suggesting differential modulation of electron transport chain components. Furthermore, dapagliflozin induced mitochondrial membrane hyperpolarization in the presence of Ca2+, with or without oligomycin, and to a lesser extent in the presence of K⁺, while no significant effects were observed under Na⁺ conditions. Collectively, these findings demonstrate that dapagliflozin directly modulates mitochondrial bioenergetics and redox balance, supporting a mechanistic link between mitochondrial function and its cardioprotective effects.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1821632</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1821632</link>
        <title><![CDATA[Effects and adaptation of high-altitude hypoxia on lipid metabolism: mechanisms and health implications]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yu Fan</author><author>WeiWei Guo</author><author>LiXin Yang</author><author>HaiQi Xu</author>
        <description><![CDATA[High-altitude environments impose substantial metabolic constraints on human physiology, with oxygen limitation driving profound alterations in lipid regulation. This narrative review synthesizes current evidence on the context-dependent effects of high-altitude hypoxia (HAH) on systemic lipid metabolism across high-altitude native populations and lowlanders exposed to altitude, with particular attention to Tibetan and Andean settings. Acute hypoxic exposure is characterized by rapid lipid mobilization, enhanced glycolytic flux, suppressed lipoprotein lipase activity, and dynamic fluctuations in circulating lipids. In contrast, acclimatization and long-term adaptation are associated with a shift toward more oxygen-efficient substrate utilization, often accompanied by reduced fatty-acid oxidation, improved insulin sensitivity, and population-specific changes in lipid profiles. However, in non-acclimatized or metabolically vulnerable individuals, sustained HAH exposure may also promote dyslipidemia, inflammation, and adverse cardiometabolic effects. By integrating evidence on HIF-mediated metabolic reprogramming, neuroendocrine regulation, genetic adaptation, and the microbiota–bile acid axis, this review highlights the heterogeneity of lipid responses to hypoxia and discusses their implications for cardiometabolic risk, preventive medicine, and future altitude-related metabolic research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1721230</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1721230</link>
        <title><![CDATA[Mitochondrial metabolic reprogramming, quality control, and intercellular transfer in regulating macrophage plasticity]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Guanheng He</author><author>Qian Sun</author>
        <description><![CDATA[Macrophage functional plasticity is intrinsically linked to metabolic reprogramming, including mitochondrial function, substrate utilization, and redox signaling. In response to hypoxia, infection, or tissue injury, macrophages rely on mitochondria not only for energy provision but, critically, for metabolic intermediates and reactive oxygen species (ROS) that serve as signaling molecules to guide gene expression reprogramming. While macrophage activation exists along a continuous spectrum, this review summarizes the distinct metabolic paradigms characterizing the classical M1-like (glycolysis-dominant) and M2-like (oxidative phosphorylation, OXPHOS-dominant) extremes, highlighting the molecular mechanisms where metabolic events—specifically tricarboxylic acid (TCA) cycle truncation and succinate accumulation—drive inflammatory polarization. Furthermore, we discuss the role of mitochondrial quality control, particularly dynamics and mitophagy, in maintaining macrophage homeostasis. Notably, recent evidence identifies “intercellular mitochondrial transfer” as a novel mode of immune microenvironment regulation, enabling damaged macrophages to restore function by acquiring exogenous mitochondria. A deeper understanding of these mechanisms offers new intervention targets for metabolic immunotherapy in sepsis, cancer, and chronic inflammatory diseases. Importantly, we emphasize that many of these metabolic and mitochondrial regulatory mechanisms are highly context-dependent, varying significantly across different tissues and disease microenvironments.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1813824</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1813824</link>
        <title><![CDATA[Pancreatitis: correcting CFTR expression and function as a promising effective treatment]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Paramita Sarkar</author><author>Wei-Yin Lin</author><author>Ava Movahed Abtahi</author><author>Woo Young Chung</author><author>Shmuel Muallem</author>
        <description><![CDATA[The two principal cell types of the exocrine pancreas, acinar and ductal cells, serve distinct but complementary roles. Acinar cells synthesize and secrete digestive enzymes, whereas duct cells secrete fluid and bicarbonate (HCO3-). Ductal secretion protects the pancreas by producing an alkaline fluid that prevents premature digestive enzyme activation and facilitates their transport to the intestine. A critical step in this protective mechanism is protein kinase A–mediated activation of the luminal Cl- channel, cystic fibrosis transmembrane conductance regulator (CFTR). In this context, increasing evidence indicates that impaired CFTR function represents a common pathological feature across all forms of pancreatitis, the most prevalent disease of the exocrine pancreas. Acute and chronic pancreatitis are inflammatory disorders characterized by pancreatic ductal injury that initiates recurrent inflammatory episodes and subsequent acinar cell damage, for which effective treatments remain lacking. Accordingly, this review aims to summarize current evidence supporting alterations in CFTR expression and activity as key events in pancreatitis pathogenesis. Furthermore, given the availability of safe and effective CFTR correctors and potentiators currently approved for the treatment of cystic fibrosis, we argue that these agents warrant strong consideration as potential therapeutic strategies for pancreatitis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1785500</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1785500</link>
        <title><![CDATA[Ductal epithelial MXD3 promotes disease progression in acute pancreatitis through Wnt/β-catenin-mediated inflammation and injury]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xianru Jia</author><author>Bingbing Cui</author><author>Xuejin Liu</author>
        <description><![CDATA[IntroductionAcute pancreatitis (AP) is a severe inflammatory disease where epithelial injury and dysregulated repair are central to pathogenesis, yet the underlying transcriptional mechanisms remain poorly understood.MethodsThis study employed an integrated approach to identify and characterize the transcription factor MXD3 as a master regulator of AP progression. Using single-cell RNA sequencing in a ceruleininduced rat AP model, we delineated a pathogenic epithelial trajectory from ciliated through non-ciliated to a proliferative state, with MXD3 emerging as the most significantly upregulated transcription factor in the proliferative cluster. Subsequent validation in pancreatic ductal epithelial-specific MXD3 knockout rats revealed profound protection against AP, manifesting as reduced histological damage, diminished fibrosis, attenuated neutrophil infiltration (MPO+ cells), and decreased expression of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β).ResultsMechanistically, we demonstrated that MXD3 directly activates the Wnt/β-catenin pathway, as evidenced by increased non-phospho β-catenin, its nuclear accumulation, and transcriptional upregulation of canonical targets (cMyc, Cyclin D1, Axin2). Furthermore, functional rescue experiments confirmed the pathway’s necessity, wherein the β-catenin inhibitor ICG-001 substantially reversed MXD3-driven apoptosis, necrosis, and pro-inflammatory cytokine secretion (IL-1β, IL-6, MCP-1) in vitro.ConclusionsOur findings establish a novel MXD3- Wnt/β-catenin axis as a crucial mechanism governing epithelial pathology in AP, revealing MXD3 as a promising therapeutic target for this debilitating condition.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1820868</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1820868</link>
        <title><![CDATA[A 2.5D multichannel deep learning model using contrast-enhanced ultrasound for predicting malignancy in breast nodules: a two-center study]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jianfeng Xie</author><author>Yan He</author><author>Jiuhe Zhu</author><author>Cuiyun Liu</author><author>Jiayuan Zhan</author><author>Lang Wang</author><author>Shaoyun Zhang</author><author>Wenjian Qin</author><author>Kun Sun</author>
        <description><![CDATA[ObjectiveTo evaluate a novel multichannel deep learning (DL) model using contrast-enhanced ultrasound (CEUS) data with multiple regions of interest (ROIs) and time-intensity curve (TIC)-derived key frames for predicting breast nodule malignancy. Clinical features were integrated into a combined model for robust, generalizable breast lesion classification. The model was further evaluated as an AI-assisted decision support tool through direct comparison with BI-RADS classification by senior radiologists.MethodsThis retrospective two-center study enrolled 141 patients with breast nodules: 89 from Institution 1 (June 2016–October 2017; training cohort, n=62; internal validation, n=27) and 52 from Institution 2 (November 2022–November 2024; external validation). BI-RADS categories were extracted from original radiology reports and binarized at ≥4B for malignancy prediction. Tumors were segmented on B-mode and CEUS images to define intratumoral ROIs, tumor bounding boxes, and peritumoral expansions (2 mm and 5 mm). TIC phases (initial, ascending, peak, descending, wash-out) were stacked into multichannel 2.5-dimensional (2.5D) inputs. DenseNet201 models, pretrained on ImageNet, were trained for 2D and 2.5D DL across ROI types. Outputs from the clinical model and optimal intratumoral plus 2-mm peritumoral ROI models were fused via logistic regression. Performance was evaluated using area under the receiver operating characteristic curve (AUC), Hosmer–Lemeshow calibration, decision curve analysis (DCA).and DeLong test for comparison with BI-RADS.ResultsAmong 2.5D models, the multichannel variant with intratumoral plus 2-mm peritumoral ROI showed highest external validation performance. The combined model, constructed by fusing the output of the optimal MultiChannel_2.5D_DL architecture (intratumoral + 2-mm peritumoral ROI) with the 2D_DL and clinical models via logistic regression, outperformed individual models externally (AUC 0.949 [95% CI: 0.888, 1.000] vs. clinical AUC 0.821 [95% CI: 0.671, 0.970], p=0.04; vs. 2D AUC 0.789 [95% CI: 0.660, 0.918], p=0.01; vs. 2.5D AUC 0.824 [95% CI: 0.677, 0.972], p=0.03). In direct comparison in the external validation cohort, the combined model demonstrated diagnostic performance comparable to that of senior radiologists (AUC 0.949 [95% CI: 0.888, 1.000] vs. 0.897 [95% CI: 0.808, 0.986], p=0.15).ConclusionThis combined model, integrating the optimal MultiChannel_2.5D_DL output with 2D_DL and clinical features, offers promising accuracy and generalizability as a decision support tool for CEUS-based breast nodule malignancy prediction, potentially assisting radiologists in reducing interobserver variability and unnecessary biopsies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1809614</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1809614</link>
        <title><![CDATA[Effects of different exercises on motor and non-motor abilities in patients with Parkinson disease—a network meta-analysis of randomized controlled trials]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Jianfeng Tang</author><author>Xinhong Liu</author><author>Jianqiang Guan</author><author>Sitao Li</author><author>Zenghui Xing</author>
        <description><![CDATA[ObjectiveTo systematically investigate and evaluate the effects of different exercise (TT: treadmill training; ST: sensorimotor training; NW: Nordic walking; CT: cycling training; WT: walking training; DT: dance training; VRT: VR training; RT: resistance training; AQT: aquatic training; BOX: boxing training; Qigong and Yoga) modalities on both motor and non-motor abilities in patients with Parkinson’s disease.MethodsRandomized controlled trials (RCTs) concerning the impact of various exercise modes on motor and non-motor abilities in Parkinson’s patients were identified by searching the PubMed, Web of Science, Cochrane library, CINAHL and CNKI databases. The search period spanned from the inception of each database to December 2025. The methodological quality of the included studies was assessed using the Cochrane Risk of Bias tool.ResultsA total of 67 RCTs involving 2642 patients were included. Network meta-analysis results indicated that WT most effectively improved UPDRS-III (SUCRA=92.5%); DT was most effective in improving TUG (SUCRA=89.9%) and 6MWT (SUCRA=73.3%); NW best improved BBS (SUCRA=91.1%) and MoCA (SUCRA=91.1%). AQT best improved PDQ-39 (SUCRA=88.5%).ConclusionCurrent evidence suggests that exercise involving walking and dance, which stimulates neural regulation, can help improve motor function and cognitive abilities in people with Parkinson’s disease. Patients can choose exercises based on their current fitness level.Systematic review registrationhttps://osf.io/7x5kc/.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1826306</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1826306</link>
        <title><![CDATA[MiR-200a-3p protects against myocardial ischemia-reperfusion injury via KEAP1–NRF2 signaling]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yanbo Zhao</author><author>Lulu Liu</author><author>Xiaohua Shen</author><author>Min Wang</author><author>Meihui Wang</author><author>Lingling Sun</author><author>Kai Zhang</author>
        <description><![CDATA[BackgroundMyocardial ischemia/reperfusion (I/R) injury is a major challenge in reperfusion therapy for acute myocardial infarction, primarily due to excessive oxidative stress, inflammation, and cardiomyocyte apoptosis. MicroRNAs are known regulators of cellular stress responses, but the role and underlying mechanism of miR-200a-3p in myocardial I/R injury remain unclear.MethodsIn vitro, hypoxia/reoxygenation (H/R) hypoxia/reoxygenation (H/R)-treated human AC16 cardiomyocytes were used to assess the effects of miR-200a-3p modulation on cell viability, apoptosis, oxidative stress, and inflammatory cytokines. The interaction with KEAP1 and downstream NRF2 activation was examined using luciferase assays and protein analyses. In vivo, cardiac-specific AAV9-mediated miR-200a-3p overexpression in mice subjected to I/R injury was evaluated for myocardial injury, oxidative stress, inflammation, apoptosis, and KEAP1–NRF2 signaling.ResultsMiR-200a-3p was markedly downregulated in H/R-treated cardiomyocytes and in mouse hearts after I/R injury. Restoring miR-200a-3p enhanced cell viability, reduced apoptosis, ROS accumulation, lipid peroxidation, and inflammatory cytokine release, and restored antioxidant defenses in vitro. In vivo, cardiac-specific miR-200a-3p overexpression attenuated myocardial injury, oxidative stress, inflammation, and cardiomyocyte apoptosis. Mechanistically, miR-200a-3p directly targeted KEAP1, promoted NRF2 nuclear translocation, and upregulated downstream antioxidant enzymes including HO-1 and NQO1, with KEAP1 suppression required for its cardioprotective effects.ConclusionThese findings indicate that miR-200a-3p protects against myocardial I/R injury by targeting KEAP1 and activating NRF2-dependent antioxidant signaling, identifying a novel redox-regulatory axis with therapeutic potential, with beneficial effects on myocardial injury and its associated functional impairment.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1793253</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1793253</link>
        <title><![CDATA[Case Report: Integrated cardiovascular and respiratory training as a novel therapeutic approach in a case of painful left bundle branch block]]></title>
        <pubdate>2026-05-01T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Oscar Crisafulli</author><author>Venere Quintiero</author><author>Caio V. Spaggiari</author><author>Anna Odone</author><author>Giuseppe D’Antona</author>
        <description><![CDATA[BackgroundLeft bundle branch block (LBBB) is a heart rate (HR)–dependent cardiac conduction disorder that may occur in the absence of structural heart disease and can be associated with painful episodes. Evidence supporting exercise-based interventions in this setting is limited. We report the case of a 41-year-old woman with paroxysmal, painful LBBB, with onset occurring marginally above resting HR.MethodsAfter a diagnostic evaluation demonstrating preserved biventricular function, absence of myocardial ischemia, and normal hemodynamic responses, a 10-month supervised training program was implemented in three sequential phases: (1) diaphragmatic breathing exercise; (2) aerobic exercise performed below the individual LBBB HR threshold; (3) interval and steady-state aerobic exercise prescribed according to individually determined ventilatory thresholds (VT1 and VT2). Resting HR, HR at LBBB onset, maximal oxygen consumption (V˙O2max), ventilatory thresholds, and their associated HRs were longitudinally assessed.ResultsAfter training, resting HR decreased by 15 bpm, while HR at LBBB onset increased by 50 bpm, markedly expanding the safe exertional window. V˙O2max improved progressively, together with upward shifts in VT1 and VT2, and reductions in corresponding HRs. Importantly, the patient reported resolution of LBBB-related pain during daily activities and even when LBBB was occasionally elicited at higher exercise intensities.ConclusionsThis case suggests that a tailored respiratory and aerobic training program may safely improve cardiovascular efficiency, functional capacity, and symptom control in a patient with painful, HR-dependent LBBB. Individualized exercise training may represent a non-invasive adjunct or alternative to pharmacological or pacing strategies in selected patients.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1787963</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1787963</link>
        <title><![CDATA[Epigenetic signatures and cellular stress response pathways in metabolic dysfunction-associated steatotic liver disease: a personalized medicine perspective]]></title>
        <pubdate>2026-04-30T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fabian M. Cortés-Mancera</author><author>Marianne G. Rots</author><author>Han Moshage</author><author>Johanna C. Arroyave-Ospina</author>
        <description><![CDATA[Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease around the world, with at least 40% global prevalence. Although genetic susceptibility contributes to disease risk, it does not fully explain the marked interindividual variability in disease onset, severity, and progression. Increasing evidence indicates that epigenetic mechanisms act as critical mediators between genetic predisposition and environmental exposures, shaping hepatic stress responses and metabolic dysfunction in MASLD. Epigenetic regulation, including DNA methylation and histone modifications, plays a fundamental role in maintaining metabolic homeostasis and coordinating cellular responses to metabolic, oxidative, and organellar stress, e.g., endoplasmic reticulum stress. Dysregulation of these processes has been consistently associated with hepatic steatosis, inflammation, fibrosis, and disease progression. Moreover, epigenetic control of circadian rhythms and molecular clock pathways further link metabolic imbalance to liver dysfunction and biological aging. Importantly, epigenetic signatures are stable, positioning them as attractive biomarkers for disease diagnosis, prognosis, and patient stratification, but also potentially reversible, making them promising targets for therapeutic intervention. Advances in epigenomic profiling and translational research are increasingly supporting the integration of epigenetic information into personalized medicine approaches for MASLD. In this review, we synthesize current experimental and translational evidence on epigenetic alterations involved in MASLD pathophysiology, with a particular focus on their role in cellular stress response pathways. We discuss the potential of epigenetic signatures as biomarkers and therapeutic targets, highlighting their relevance for the development of precision-based strategies in the management of MASLD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1820693</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1820693</link>
        <title><![CDATA[Analysis of player heart rate and stroke success in tennis drill scenarios]]></title>
        <pubdate>2026-04-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ibrahim Cem Balci</author><author>Buse Cicek</author><author>Irem Sayin</author><author>Serkan Salturk</author><author>Onur Sarialioglu</author><author>Deniz Ozel</author><author>Nika Kakulia</author><author>Ali Anil Demircali</author><author>Huseyin Uvet</author>
        <description><![CDATA[Heart rate (HR) is a practical indicator of physiological load and arousal, yet its shot by shot relationship with tennis performance remains insufficiently characterized. We quantified associations between HR and stroke outcome and spatial accuracy during a standardized target based drill. The dataset comprised 8,197 shots from 23 players across 93 training sessions. HR was sampled at 1 Hz and temporally aligned to each shot using a fixed ±5 s window around the shot reference time, enabling the extraction of absolute HR levels, short term HR changes and HR intensity zones. Shot outcomes (successful/unsuccessful) and distance to the nearest target area corner were obtained using a camera based tracking system. Successful strokes were generally associated with lower HR levels (p< 0.001; small effects, r ≈ 0.17). Short term HR dynamics provided limited additional discrimination, with only pre-shot change showing a small difference between outcomes. HR intensity zones were associated with success (p< 0.001), with a greater proportion of successful strokes occurring in lower zones (Zones 1-3). Accounting for repeated shots within sessions and players, mixed-effects models were additionally fitted. Higher HR remained associated with lower odds of shot success (OR per 10 bpm = 0.957, 95% CI 0.953-0.961) and a model using heart rate at the shot instant yielded very similar estimates. The continuous distance outcome showed weaker evidence after hierarchical adjustment. Overall, shot-aligned HR monitoring may provide useful contextual information for interpreting performance during precision-focused drills. However, the modest effect sizes suggest that HR should be considered alongside technical and task-related indicators rather than as a primary basis for training decisions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1785483</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1785483</link>
        <title><![CDATA[Physiological responses and adaptive mechanisms of amphibians and reptiles to multiple interacting environmental stressors: an integrative review]]></title>
        <pubdate>2026-04-30T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Muammer Kurnaz</author>
        <description><![CDATA[This integrative review synthesizes current knowledge on the physiological responses and adaptive mechanisms of amphibians and reptiles to multiple interacting environmental stressors, with particular emphasis on synergistic effects among temperature, hydric stress, disease, and pollution. Given the stronger empirical basis for amphibians in the existing literature, amphibian responses are covered in greater depth, while reptile-specific physiology, immunology, and emerging infectious diseases are explicitly addressed in dedicated sections throughout the review. Critical thermal tolerance analyses reveal that approximately 7.5% of amphibian species will exceed their physiological limits under a 4 °C warming scenario, with tropical lowland species already operating near their CTmax thresholds. Thermal plasticity is limited, with acclimation responses averaging only 0.13 °C increase in CTmax per 1 °C environmental warming—insufficient to track rapid climate change. Water balance regulation shows dramatic interspecific variation, with cutaneous resistance ranging from 0.05 s/cm in aquatic amphibians to >1000 s/cm in desert-adapted reptiles. Synergistic interactions between thermal and hydric stress significantly amplify vulnerability, particularly in dehydration scenarios that reduce critical thermal limits. Chemical pollutants, including heavy metals and pesticides, cause developmental abnormalities (535% increase in malformation frequency), immunosuppression, and endocrine disruption across multiple life stages. Emerging infectious diseases, particularly chytridiomycosis (Batrachochytrium dendrobatidis and B. salamandrivorans) and ranaviruses, drive mass mortality events globally, with co-infections exacerbating population declines. Climate change intensifies disease susceptibility through stress-mediated immunosuppression and altered pathogen dynamics. Adaptive capacity varies markedly among species. While amphibians exhibit strong phenological responses (2-4× greater than other taxa), genetic adaptation potential remains limited by narrow dispersal abilities and habitat fragmentation. Microhabitat buffering can reduce thermal extremes by several degrees but depends critically on habitat structural integrity. This review demonstrates that the pace of anthropogenic change challenges the adaptive capacity of most species, necessitating integrated conservation strategies including microhabitat preservation, climate corridor establishment, pollution mitigation, disease surveillance, and ex-situ conservation programs.]]></description>
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