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        <title>Frontiers in Physiology | Redox Physiology section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/physiology/sections/redox-physiology</link>
        <description>RSS Feed for Redox Physiology section in the Frontiers in Physiology journal | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-13T19:51:55.735+00:00</pubDate>
        <ttl>60</ttl>
        <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>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1849826</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1849826</link>
        <title><![CDATA[Editorial: Pharmacodynamic and pharmacokinetic aspects of redox signaling in inflammation-associated damage and diseases]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Mamunur Rashid</author><author>Siva Rama Raju Kanumuri</author><author>Mohd Yaseen Malik</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1796160</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1796160</link>
        <title><![CDATA[Methyl eugenol attenuates age-associated oxidative fragility by coupling Ca2+-calpain inhibition with Band 3 stabilization in human erythrocytes]]></title>
        <pubdate>2026-04-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jiasi Zhang</author><author>Qingwen Li</author><author>Yilan Dai</author><author>Shuaiheng Hou</author><author>Xuan Peng</author><author>Ji Zhang</author><author>Nianqiao Gong</author>
        <description><![CDATA[BackgroundHuman erythrocytes serve as an ideal model for cellular aging, a process where longevity relies on membrane scaffold integrity. The oxidative deterioration of Band 3, a major integral membrane protein, is a central driver of this senescence. This study investigated whether methyl eugenol (ME) stabilizes Band 3 against age-associated oxidative fragility.MethodsErythrocytes were challenged with H2O2 to simulate age-associated oxidative injury. Damage was evaluated via hemolysis assays, SEM, and flow cytometry. Sulfate (SO42-) uptake kinetics and Western blotting were employed to assess Band 3 anion exchange function and structural stability. In silico docking simulated interactions between ME metabolites and the Band 3 structure. Physiological relevance was validated in a human cohort (n = 81; 20–90 years) via regression and stratified analyses of glutathione (GSH) and malondialdehyde (MDA) levels.ResultsME exhibited an optimal protective concentration at 2 µM, effectively preserving biconcave morphology and attenuating hemolysis. Treatment significantly mitigated intracellular oxidative stress and rescued cell viability. Mechanistically, ME suppressed the pathological increase in intracellular Ca2+ concentration and inhibited calpain activity. Functionally, ME significantly restored sulfate transport rates. Western blotting confirmed that ME specifically preserved the full-length (100 kDa) and cytoplasmic (43 kDa) domains of Band 3, whereas the 55 kDa transmembrane domain remained largely unaffected. Docking simulations predicted a specific interaction with residue ARG292 within the cytoplasmic domain, suggesting a structural basis for this stabilization. In the donor cohort, ME extended the projected GSH half-life (from 47.14 to 64.14 years) and reduced maximal lipid peroxidation by ~40%.ConclusionME mitigates oxidative eryptosis by coupling Ca2+–calpain inhibition with site-specific Band 3 stabilization, offering a rationale for using ME to standardize erythrocyte quality and reduce age-associated fragility.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1756889</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1756889</link>
        <title><![CDATA[Optimization, characterization, and protective potentials of Periploca angustifolia extract against cadmium toxicity using response surface methodology as an optimizing tool]]></title>
        <pubdate>2026-04-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Imen Ben Abdelmalek</author><author>Khaled Athmouni</author><author>Saida S. Ncibi</author><author>Ghadah Khaled Yousuf</author><author>Maha Smaouia</author><author>Hanen Enneb</author><author>Abdelfattah El Feki</author>
        <description><![CDATA[IntroductionPhenolic compounds isolated from medicinal plants are used against several physiological disorders.MethodsIn this investigation, microwave-assisted extraction parameters were optimized using response surface methodology (RSM) to determine the optimal extraction conditions for phenolic compounds from Periploca angustifolia extract (PAPE). The phenolic extract was characterized by nuclear magnetic resonance (NMR) spectroscopy. The antioxidant activity of the extract was evaluated using standard antioxidant assays. In addition, the protective effect of the phenolic extract was evaluated against cadmium toxicity.Results and discussionOur analysis showed that the optimum extraction conditions were an irradiation time of 10 min, an extraction temperature of 100 °C, and a water-to-raw-material ratio of 30 mL/g. HPLC analysis indicated that PAPE contained quercetin, catechin, and caffeic acid. NMR (1D and 2D) spectra confirmed the compounds identified by HPLC. Antioxidant assays showed that PAPE exhibited a strong free-radical scavenging ability. In vivo analysis showed that PAPE produced a significant (p < 0.01) protective effect against oxidative damage induced by cadmium exposure in rat testicles. In conclusion, PAPE demonstrated strong antioxidant potential that is likely attributable to the active compounds present in the extract.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1783080</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1783080</link>
        <title><![CDATA[Modulation of the serotonergic system restores oxidative balance and gene expression in the brain and heart of rats with obesity induced by overnutrition]]></title>
        <pubdate>2026-04-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Maria Daniele Teixeira Beltrão de Lemos</author><author>Matheus Santos de Sousa Fernandes</author><author>Thyago de Oliveira Rodrigues</author><author>Vanessa Lima de Souza</author><author>Fatma Hilal Yagin</author><author>Severina Cássia de Andrade Silva</author><author>Osmar Henrique dos Santos Junior</author><author>Diorginis José Soares Ferreira</author><author>Monira I. Aldhahi</author><author>Claudia J. Lagranha</author>
        <description><![CDATA[IntroductionStudies have demonstrated that insults during development increase the risk for developing diseases later in life, including hypertension, ischemic heart disease, stroke, respiratory disease, diabetes, cancer, as well as psychiatric disorders. Hence, as mitochondrial dysfunction-induced oxidative stress has been proposed to be a central molecular hub linking metabolic and oxidative stress pathways, the serotonin modulation-related mitochondrial boost might mitigate such impairments. Thus, the present study investigates the effects of serotonina modulation by uoxetine on oxidative stress and mitochondrial biogenesis biomarkers in the brainstem and heart of male rats that were overfed during lactation period.MethodsNormo and overfed animals received uoxetine (FX, SSRI) or saline from postnatal day 39 to postnatal day 59, wherein tissues were collected 24 hours later.Results and discussionOverfeeding increased body weight and induced lipid peroxidation and protein oxidation in both tissues, while genes related to mitochondrial dynamics (PGC1a and TFAM) were speci cally modulated, suggesting a targeted effect of uoxetine on mitochondrial biogenesis pathways by overfeeding across the tissues. Together, our results suggest that early life overfeeding deregulates oxidative balance and mitochondrial biogenesis, wherein FX administration acts toward molecular normalization both in heart and brainstem of male offspring. These ndings shed light on the potential of serotonin modulation to mitigate the effects of overnutrition during developmental periods.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1772933</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1772933</link>
        <title><![CDATA[MsrB2 deficiency amplifies ECM-driven cardiac fibrosis under hypertensive stress]]></title>
        <pubdate>2026-03-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ji Ho Yun</author><author>Suyeon Cho</author><author>Jong Youl Lee</author><author>Suji Kim</author><author>Seung Hee Lee</author>
        <description><![CDATA[BackgroundMethionine sulfoxide reductase B2 (MsrB2), a mitochondrial redox enzyme essential for maintaining protein integrity under oxidative stress, has been implicated in diabetic cardiac remodeling. However, its contribution to hypertension-induced fibrosis remains unclear. Hypertension frequently coexists with diabetes and accelerates cardiac fibrotic remodeling, particularly in non-obese diabetic patients who may exhibit distinct metabolic and oxidative responses.MethodsWe investigated the role of MsrB2 in extracellular matrix (ECM)-driven cardiac fibrosis using both animal and human hypertensive heart samples. MsrB2 expression was evaluated in non-obese (Goto-Kakizaki, GOTO) and obese (OLETF) diabetic rat models and in angiotensin II (Ang II)–infused MsrB2 knockout (KO) mice. Histological, biochemical, and transcriptomic analyses were performed to assess myocardial fibrosis, fibrosis-related signaling, and redox gene expression.ResultsMsrB2 expression was markedly reduced in human hypertensive hearts and in the myocardium of non-obese diabetic rats, whereas it remained unchanged in obese diabetes despite similar increases in blood pressure. In MsrB2 KO mice, Ang II infusion provoked extensive interstitial and perivascular collagen deposition, accompanied by enhanced SMAD2/3 activation and upregulation of profibrotic ECM genes including Col1a1, Col3a1, COMP, and LOX. Transcriptomic profiling revealed strong enrichment of extracellular matrix and collagen-related pathways, along with increased expression of oxidative/inflammatory mediators such as Spp1 and Ccr2, while antioxidant and mitochondrial quality-control genes (Sdhaf2, Rnls, Mapk8) were suppressed. These results indicate that MsrB2 deficiency shifts the myocardium toward a pro-oxidant and pro-fibrotic phenotype under hypertensive stress.ConclusionLoss of MsrB2 amplifies ECM-driven cardiac fibrosis during hypertensive stress by promoting oxidative imbalance and SMAD2/3 activation. In non-obese diabetes, the concomitant reduction of MsrB2 expression may further accelerate hypertensive remodeling, highlighting a mechanism that could explain the higher incidence of cardiovascular complications observed in non-obese diabetic individuals. These findings identify MsrB2 as a critical redox regulator that restrains ECM-driven fibrosis and suggest that enhancing its activity could represent a therapeutic approach to prevent metabolic and hypertensive cardiac disease.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1734890</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1734890</link>
        <title><![CDATA[Redox signaling in chronic airway diseases: pathogenic mechanisms and therapeutic implications]]></title>
        <pubdate>2026-03-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Mario Cazzola</author><author>Paola Rogliani</author><author>Luigino Calzetta</author><author>Frank M. P. van Haren</author><author>Clive Page</author><author>Maria Gabriella Matera</author>
        <description><![CDATA[Chronic airway diseases, including asthma, chronic obstructive pulmonary disease (COPD), and bronchiectasis, impose a significant global health burden. A central unifying feature of these diseases is redox imbalance, which is characterized by an excess of reactive oxygen and nitrogen species (ROS/RNS) that overwhelms the body’s antioxidant defenses, causing cellular dysfunction, inflammation, and tissue damage. Physiological ROS/RNS are essential for immune regulation and transcriptional control, but chronic oxidative stress disrupts these processes, driving disease progression. In asthma, eosinophil- and epithelial-derived ROS worsen airway hyperresponsiveness, induce mucus overproduction, and reduce steroid effects. COPD involves neutrophil-dominated inflammation, mitochondrial dysfunction, protease- and oxidant-mediated extracellular matrix degradation, and accelerated senescence. Bronchiectasis features persistent neutrophilic oxidative injury, microbial colonization, impaired mucociliary clearance, and progressive airway destruction. Exogenous oxidants, cigarette smoke, biomass fuels, pollutants, and pathogens further burden antioxidant systems, including superoxide dismutases, catalase, glutathione peroxidase, and Nrf2-regulated pathways. Redox dysregulation also contributes to post-COVID sequelae, promoting ongoing airway inflammation, fibrosis, and systemic complications. Therapeutic strategies targeting redox imbalance, mainly thiol-based antioxidants, Nrf2 activators, NADPH oxidase inhibitors, and mitochondria-targeted antioxidants, show mechanistic promise but face challenges in specificity, bioavailability, and clinical translation. Advancing precision redox medicine requires biomarker-guided patient stratification, high-resolution redox proteomics, single-cell and organoid models, and spatial imaging to identify disease-specific redox endotypes. Modulating pathological oxidative stress while preserving physiological signaling offers a novel avenue to improve outcomes. Understanding redox biology in airway disease highlights the potential of precision antioxidant strategies as adjuncts to conventional therapies, representing a paradigm shift in managing chronic airway disorders.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1779008</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1779008</link>
        <title><![CDATA[Systematic review and meta-analysis of antioxidant treatment in patients with acute mountain sickness induced by high altitude exposure]]></title>
        <pubdate>2026-03-09T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Eduardo Pena</author><author>Alexandra Del Río</author><author>Sergio Flores</author>
        <description><![CDATA[Acute Mountain Sickness (AMS) is a frequent condition triggered by exposure to hypobaric hypoxia at high altitude. Its pathophysiology involves endothelial dysfunction and oxidative stress, with elevated oxidative molecules identified as key contributors to its development. Antioxidant therapies such as vitamins C/E, α-lipoic acid, and Ginkgo biloba have been proposed, though results across studies remain inconsistent.ObjectiveThis study aims to evaluate the effects of antioxidant treatments in subjects with AMS induced by high-altitude exposure, examining their impact on clinical outcomes and oxidative stress markers.MethodsA systematic review and meta-analysis were performed according to PRISMA2020 guidelines. Searches were conducted in PubMed, Scopus, and Web of Science through November 2025, supplemented by snowball methods, focusing on studies investigating antioxidant treatments in humans exposed to hypobaric or high-altitude hypoxia. Inclusion criteria were original research in English with full-text availability, human exposure to hypobaric hypoxia, AMS assessment using the Lake Louise Score (LLS), and explicit antioxidant interventions compared with placebo or control. A random-effects meta-analysis using the REML estimator was applied to calculate relative risk (RR), including continuity corrections for zero-event studies. Data extraction was performed in duplicate, and risk of bias was evaluated using the Cochrane tool.ResultsThe search yielded 727 records; nineteen studies were included in the qualitative synthesis, and four trials provided comparable dichotomous data for quantitative analysis. Pooled estimates showed a non-significant trend toward reduced AMS incidence with antioxidant treatment (RR ≈ 0.73; 95% CI: 0.47–1.11; p = 0.14). Moderate heterogeneity was detected (I2 = 52%, Q p = 0.048). Although not statistically significant, all studies showed a direction of effect favoring antioxidants. Nevertheless, interpretation is limited using pre-2018 LLS diagnostic criteria, absence of studies under chronic intermittent hypobaric hypoxia, and methodological variability.ConclusionCurrent evidence does not demonstrate a statistically significant protective effect of antioxidant therapy against AMS; however, findings remain inconclusive due to few available trials, small sample sizes, pharmacokinetics and pharmacodynamics analysis, and methodological heterogeneity. Larger, well-designed trials with standardized ascent profiles and redox biomarkers are required to determine clinical efficacy.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420261331390, identifier CRD420261331390.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1764165</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1764165</link>
        <title><![CDATA[Enzymes that generate and regulate intracellular persulfides and polysulfides: mechanistic insights and inhibitors]]></title>
        <pubdate>2026-02-09T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Ko Hirabayashi</author><author>Eita Sasaki</author><author>Hisashi Ohno</author><author>Orie Takayama</author><author>Sota Yamada</author><author>Kenjiro Hanaoka</author>
        <description><![CDATA[Reactive sulfur species (RSS), which include various persulfides and polysulfides, are generated by multiple enzymes in vivo and play critical roles in mammalian physiological processes such as redox signaling, metabolic regulation, radical scavenging and anti-inflammatory responses. Cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3MST) are well known to mediate endogenous production of hydrogen sulfide (H2S), and, together with the mitochondrial isoform of cysteinyl-tRNA synthetase (CARS2), are proposed to be major sources of intracellular persulfides and polysulfides. In mitochondria, enzymes involved in the sulfide oxidation pathway, including sulfide:quinone oxidoreductase (SQOR), persulfide dioxygenase (ETHE1) and thiosulfate sulfurtransferase (TST), also contribute to maintaining and regulating intracellular persulfide levels. Selective inhibitors targeting these enzymes are expected to be powerful tools for elucidating the functions of RSS, as well as having therapeutic potential. In this review, we present a comprehensive overview of these enzymes, focusing on their reaction mechanisms and inhibitors.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1767235</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1767235</link>
        <title><![CDATA[AB-Flu nanodrug combined with exercise intervention enhances ROS-mediated antitumor effects in melanoma]]></title>
        <pubdate>2026-02-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yuanbing Zhou</author><author>Jinke Ma</author><author>Ziyu Zhang</author><author>Xiaodan Niu</author><author>Huiyu Yan</author><author>Jun Zhang</author>
        <description><![CDATA[PurposeThis study aims to investigate the synergistic effects of AB-Flu nanodrugs and exercise intervention on enhancing the antitumor effects in melanoma by improving the hypoxic tumor microenvironment (TME). The focus is on evaluating how this combination influences reactive oxygen species (ROS) levels, inhibition of melanoma in vivo.MethodsAn intact B16F10 melanoma mouse model was established, and mice were divided into four groups: control, AB-Flu treatment, exercise intervention, and combination therapy (AB-Flu + exercise). AB-Flu nanodrug was administered intraperitoneally, while exercise was facilitated by a weighted swimming intervention. Tumor growth, tumor hypoxia, ROS levels, and apoptosis were analyzed through tumor volume measurements, histological staining, and ROS detection assays. The antitumor effects of different treatments were compared.ResultsThe combination therapy group showed the most significant tumor inhibition efficacy with tumor growth inhibition rates of 56%, compared to 30% for the AB-Flu monotherapy group and 41% for the exercise group. Additionally, tumor tissues from the combination group exhibited significantly lower levels of hypoxia and enhanced tumor cell apoptosis. ROS levels were substantially higher in the combination therapy group compared to other groups, indicating that the combination of AB-Flu and exercise synergistically elevated ROS production, which may contribute to increased tumor cell apoptosis. No significant toxicity was observed in major organs.ConclusionThe combination of AB-Flu nanodrugs and exercise intervention significantly enhances the antitumor effects in melanoma by improving the hypoxic TME, elevating ROS levels, and promoting apoptosis in tumor cells. This strategy may offer a potential approach for melanoma therapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1733194</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1733194</link>
        <title><![CDATA[Oxidative stress-mediated responses in endometrial cancer cells: contrasting effects of doxorubicin and menadione]]></title>
        <pubdate>2026-02-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Joanna Kozak</author><author>Sandra Tkaczyk–Beraś</author><author>Krzysztof Jędraszek</author>
        <description><![CDATA[BackgroundOxidative stress plays a crucial role in the development and treatment response of endometrial cancer, yet the antioxidant defense mechanisms in different tumor subtypes remain unclear.MethodsWe investigated the cellular response to oxidative (menadione) and genotoxic (doxorubicin) stress in two TP53-mutated endometrial cancer cell lines, AN3CA and KLE. Cell viability, reactive oxygen species (ROS) levels, and the expression of antioxidant-related genes (SESN2, SESN3, SOD1) were assessed using qPCR and In-Cell Western assays.ResultsAN3CA cells showed greater sensitivity to doxorubicin, marked by increased ROS and reduced viability, while KLE cells were more susceptible to menadione-induced toxicity. Protein expression analysis revealed a biphasic response: low doses of doxorubicin transiently increased SESN and SOD1 expression, whereas higher doses suppressed them. Gene expression at the mRNA level did not always correlate with protein levels, suggesting possible post-transcriptional regulation.ConclusionOur findings demonstrate cell line - specific redox responses and identify SESN2, SESN3, and SOD1 as key players in the antioxidant defense network. These genes may serve as potential therapeutic targets in aggressive, hormone-independent endometrial cancers.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2026.1779024</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2026.1779024</link>
        <title><![CDATA[Editorial: Spotlight on nitric oxide: integrative approaches to study NO and RNS in physiology and disease]]></title>
        <pubdate>2026-01-29T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Erika M. Palmieri</author><author>Andrew Gow</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1719454</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1719454</link>
        <title><![CDATA[Effects of regular exercise on ischemia-modified albumin and total sulfhydryl levels in young women: a cross-sectional study]]></title>
        <pubdate>2025-11-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ömer Faruk Bilici</author><author>Muhammed Zahit Kahraman</author><author>Ali Türker</author><author>Sinan Seyhan</author><author>Mehmet Furkan Sahin</author><author>Halit Demir</author><author>Görkem Acar</author><author>Muhammed Fatih Bilici</author><author>Caglar Soylu</author><author>Tarkan Söğüt</author><author>Abdullah Bakum</author>
        <description><![CDATA[BackgroundRegular physical activity provides systemic health benefits, including improvements in redox homeostasis and antioxidant defense. Ischemia-modified albumin (IMA) and total sulfhydryl groups (–SH) serve as sensitive biomarkers of oxidative protein modification and thiol-dependent antioxidant capacity. However, evidence regarding their relationship in young women who participate in structured exercise remains limited. This study aimed to investigate associations between regular exercise and serum IMA and –SH concentrations in healthy young women to better understand potential exercise-related redox differences and sex-specific physiological profiles.MethodsThis cross-sectional study included 30 healthy women aged 18–25 years, recruited from university campuses and local fitness facilities. Participants were assigned to an exercise group (n = 15), performing structured training ≥3 sessions per week for at least 1 year, or a sedentary control group (n = 15) with no structured exercise history. After ethical approval and informed consent, venous blood samples were drawn following overnight fasting. Serum IMA was measured using the albumin–cobalt binding assay, while –SH concentrations were determined via the Ellman method. All analyses were conducted in duplicate under standardized laboratory conditions. Independent samples t-tests and Cohen’s d effect sizes with 95% confidence intervals were calculated.ResultsBaseline anthropometric variables (age, height, weight) did not differ significantly between groups (p > 0.05). Serum IMA levels were significantly higher in the exercise group than in controls (0.75 ± 0.09 vs. 0.61 ± 0.08 ABSU; p < 0.001; d = 1.65). Conversely, –SH concentrations were significantly lower among exercising women (0.370 ± 0.046 vs. 0.447 ± 0.036 mmol/L; p < 0.001; d = −1.88). Both biomarkers showed very large effect sizes, reflecting robust differences in oxidative stress and antioxidant defense associated with regular physical training.ConclusionThis cross-sectional analysis indicates that regular structured exercise in young women is associated with a distinct redox profile characterized by elevated IMA and reduced –SH levels. This dual pattern may reflect altered redox homeostasis with increased oxidative protein modification and greater thiol utilization. IMA and –SH appear to be complementary biomarkers for evaluating exercise-related redox responses. Future longitudinal studies are needed to establish causal mechanisms and clinical significance.Clinical Trial RegistrationRegistered at ClinicalTrials.gov (NCT07181044) on 6 September 2025.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1666999</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1666999</link>
        <title><![CDATA[Activation of the pentose phosphate pathway by microcurrent stimulation mediates antioxidant effects in inflammation-stimulated macrophages]]></title>
        <pubdate>2025-11-14T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mikiko Uemura</author><author>Noriaki Maeshige</author><author>Atomu Yamaguchi</author><author>Xiaoqi Ma</author><author>Yunfei Fu</author><author>Taketo Inoue</author><author>Mami Matsuda</author><author>Yuya Nishimura</author><author>Tomohisa Hasunuma</author><author>Ji Wang</author><author>Hiroyo Kondo</author><author>Hidemi Fujino</author>
        <description><![CDATA[IntroductionExcessive inflammatory responses in macrophages lead to increased oxidative stress, and the excessive production of reactive oxygen species (ROS) causes tissue damage, contributing to the development of chronic diseases and tissue deterioration. Therefore, controlling the inflammatory response and ROS production is crucial for human health. Electrical stimulation (ES) has been shown to have antioxidant and anti-inflammatory effects on macrophages. However, the key pathway underlying these effects remains unclear.MethodsIn this study, ES was applied to Lipopolysaccharide (LPS)-stimulated macrophages, and the production of ROS and 8–hydroxy–2′–deoxyguanosine (8-OHdG), inflammatory cytokine expression, and intracellular metabolites were analyzed in a glucose-6-phosphate dehydrogenase (G6PD) knockdown experiment, the rate-limiting enzyme of the Pentose Phosphate Pathway(PPP).ResultsES significantly increased sedoheptulose 7-phosphate (S7P), an intermediate metabolite in PPP, and reduced ROS and 8-OHdG production and the expression of inflammatory cytokines in LPS-stimulated macrophages. Meanwhile, ES did not exert antioxidant effects in G6PD-knockdown macrophages.DiscussionThese findings indicate that the antioxidant effects of ES are mediated by PPP in LPS-stimulated macrophages.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1695456</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1695456</link>
        <title><![CDATA[Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice]]></title>
        <pubdate>2025-11-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Helena Hernández-Cuervo</author><author>Ramani Soundararajan</author><author>Sahebgowda Sidramagowda Patil</author><author>Mason T. Breitzig</author><author>Matthew Alleyn</author><author>Venkata Ramireddy Narala</author><author>Richard Lockey</author><author>Lakshmi Galam</author><author>Narasaiah Kolliputi</author>
        <description><![CDATA[IntroductionAdministering high levels of oxygen is a life-sustaining measure in critically ill lung subjects. However, prolonged hyperoxia exposure increases reactive oxygen species (ROS) that exacerbate oxidative stress, mitochondrial dysfunction, respiratory failure, and cell death. Mitochondria play a critical role in hyperoxia-induced acute lung injury (HALI). The specific role of the Polycomb Repressive Complex 1 protein BMI1 (B cell-specific Moloney murine leukemia virus integration site 1) in mitochondrial damage remains unknown.MethodsBmi1 knockout mice (Bmi1−/−) and their wild-type (WT) littermates were exposed to normobaric hyperoxia using oxygen concentrations of 95-100% for 48 h to assess BMI1 function in HALI. This research included the estimation of protein and gene expression, live mitochondria isolation, Oxygen consumption rate measurement, histomorphology analysis, capillary assessment, and dynamic lung function evaluation.ResultsMice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance.DiscussionBmi1−/− mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. Our results indicate that Bmi1−/− mice are susceptible to HALI, and the damage increases in those mice compared with their WT littermates.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1426102</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1426102</link>
        <title><![CDATA[Nitroalkene inhibition of pro-inflammatory macrophage effector function via modulation of signaling metabolite levels]]></title>
        <pubdate>2025-10-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Emily R. Stevenson</author><author>James P. O’Brien</author><author>Allison M. Manuel</author><author>Crystal E. Uvalle</author><author>Gregory J. Buchan</author><author>Steven J. Mullett</author><author>Karina Lockwood</author><author>Tomeka Suber</author><author>Bruce A. Freeman</author><author>Stacy L. Gelhaus</author>
        <description><![CDATA[IntroductionClassically activated innate immune cells undergo a metabolic switch to aerobic glycolysis to support effector function. We report that the small-molecule nitroalkene 10-n-octadec-9-enoic acid (NO2-OA) attenuates the Warburg- like phenotype of aerobic glycolysis in lipopolysaccharide (LPS)-activated macrophages, thus inhibiting pro-inflammatory signaling.MethodsRAW264.7 and bone marrow derived macrophage were treated with LPS with and without NO2-OA or 1400W. Pro-inflammatory cytokines were measured by ELISA and protein expression was determined by immunoblot. Central carbon metabolites with and without 13C stable isotope tracing were measured using liquid chromatography-high resolution mass spectrometry.ResultsOverall, the present observations indicate that nitroalkene-induced changes in central carbon metabolism contribute to the anti-inflammatory actions of this class of multi-target lipid signaling mediators. Comparison of macrophage responses to NO2-OA with the inducible nitric oxide synthase (NOS2 and iNOS) inhibitor 1400W affirms that NO2-OA inhibition of NOS2 expression and activity alone was not sufficient to account for the decreases in pro-inflammatory cytokine expression. NO2-OA treatment reduced intracellular succinate levels, which may be attributed to a concomitant reduction in intracellular itaconate and reliance on glutamine, thereby contributing to hypoxia-inducible factor 1α (HIF1α) destabilization observed in LPS-activated macrophages.ConclusionThe current data provide additional perspective on the actions of this small-molecule electrophile, which is currently in a Phase 2 clinical trial for the treatment of obesity-related chronic pulmonary inflammation and associated airway dysfunction.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1567603</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1567603</link>
        <title><![CDATA[How does exercise regulate the physiological responses of post traumatic stress disorder? the crosstalk between oxidative stress and the hypothalamic-pituitary-adrenal axis]]></title>
        <pubdate>2025-09-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Tianyu Zhang</author><author>Jianda Kong</author>
        <description><![CDATA[Post traumatic stress disorder (PTSD) is a severe psychological disorder cautilized by extreme traumatic events, typically accompanied by physiological mechanisms, such as oxidative stress and dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis. Our review explores how exercise boosts the physiological response of PTSD patients by regulating oxidative stress and HPA axis function, and delves into the potential mechanisms and application prospects of exercise in PTSD treatment. By a review of existing literature, we mainly discussed the effects of various types of exercise, like aerobic exercise, strength training, and high-intensity interval training (HIIT), on oxidative stress markers and HPA axis function, and evaluated the efficacy and mechanism of exercise intervention in the treatment of post traumatic stress disorder. Specifically, regular exercise can enhance the antioxidant defense system, reduce levels of reactive oxygen species (ROS), restore HPA axis function, and thereby alleviate the psychological and physiological symptoms of post-traumatic stress disorder. Different types of exercise have varying influences on the regulation of oxidative stress and cortisol secretion patterns. As a multidimensional therapeutic approach, exercise can provide comprehensive therapeutic advantages by enhancing neural plasticity, promoting immune function, and improving psychological resilience. In addition, the combination of exercise with conventional treatment strategies, such as cognitive-behavioral therapy and medication has apparently optimized treatment outcomes.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1641354</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1641354</link>
        <title><![CDATA[Correction: Endothelial AIP1 regulates vascular remodeling by suppressing NADPH Oxidase-2]]></title>
        <pubdate>2025-08-04T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Jiqin Zhang</author><author>Chaofei Chen</author><author>Li Li</author><author>Huanjiao J. Zhou</author><author>Fenghe Li</author><author>Haifeng Zhang</author><author>Luyang Yu</author><author>Yuxin Chen</author><author>Wang Min</author>
        <description></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1485367</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1485367</link>
        <title><![CDATA[Oxidative stress in periodontitis and the application of antioxidants in treatment: a narrative review]]></title>
        <pubdate>2025-05-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Wei Liu</author><author>Daoyu Guo</author>
        <description><![CDATA[Periodontitis has turned into a general oral disease defined by chronic inflammation of the gums and helping tissues of the teeth. It dramatically influences both oral and systemic health and is a main trigger of tooth loss. Periodontitis is tightly linked to oxidative stress, and evidence reveals the utilization of certain antioxidants in related treatments. Our review delves into literature in periodontitis, centering on the latest therapeutic strategies and mechanistic evidences. This review starts by depicting the epidemiological features and pathogenic mechanisms of periodontitis, highlighting the vital mechanism of microbial community modefications, host immune responses, and genetic factors in disease development. Existing treatment approaches for periodontitis involve mechanical cleaning, antibiotic therapy, surgical interventions, and pharmacological treatments, with a comprehensive exploration on the strengths and limitations of each strategy and their related clinical utilizations. Besides, this review investigates emerging therapies, like anti-inflammatory treatments, immune modulation therapies, and biotechnological utilization in the control of periodontitis. It particularly stresses the protective effects of antioxidants and their mechanistic researches in periodontitis, highlighting their potential in slowing inflammatory responses and boosting tissue repair. Ultimately, our review intends to the concept of individual therapy and investigates future directions, comprising the utilization of precision medicine in periodontitis control and the individual design of treatment utilization.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fphys.2025.1551932</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fphys.2025.1551932</link>
        <title><![CDATA[Hemoglobin-based oxygen carriers, oxidative stress and myocardial infarction]]></title>
        <pubdate>2025-04-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Timothy N. Estep</author>
        <description><![CDATA[IntroductionDevelopment of hemoglobin-based oxygen carriers (HBOCs) for use as temporary blood replacement solutions and treatment of hemorrhagic shock has been hindered because of evidence HBOC infusion increases the risk of myocardial infarction (MI).MethodsTo gain insight into potential toxicity mechanisms, MI incidence from later stage clinical testing of five HBOCs was compared to pharmacokinetic and biochemical parameters to identify correlations suggestive of cause-and-effect hypotheses.ResultsThere are positive correlations between MI incidence and HBOC dose, size, intravascular half-life and area under the plasma concentration versus time curve (AUC). Furthermore, MI incidence is positively correlated with initial rates of HBOC autoxidation, oxidation by nitric oxide, and AUCs estimated for these HBOC oxidation products.ConclusionsThese observations imply that increased MI risk after HBOC infusion is due to intravascular reactions which exacerbate oxidative stress.]]></description>
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