Redox Biology最新文献

{"title":"Patient-derived lung organoids from bronchoalveolar lavage capture epithelial heterogeneity and disease biology in bronchopulmonary dysplasia","authors":"Shilpa Sonti ,&nbsp;Abiud Cantu ,&nbsp;Manuel Cantu Guttierez ,&nbsp;Connor Leek ,&nbsp;Phinzy Pelton ,&nbsp;Erik A. Jensen ,&nbsp;Krithika Lingappan","doi":"10.1016/j.redox.2026.104057","DOIUrl":"10.1016/j.redox.2026.104057","url":null,"abstract":"<div><div>Modeling neonatal lung disease <em>ex vivo</em> to elucidate disease pathogenesis is particularly challenging. We hypothesized that airway organoids derived from bronchoalveolar lavage (BAL) samples obtained from intubated preterm infants with bronchopulmonary dysplasia (BPD) will recapitulate the epithelial heterogeneity seen in human airways and can be used to study lung injury and therapeutic responses. Here, we demonstrate that BAL sample-derived airway organoids from ventilator-dependent patients with established BPD exhibited cellular heterogeneity consistent with that observed in the human airway. Developed organoids contain basal cell progenitors and a spectrum of differentiated epithelial subtypes, including secretory, ciliated, PNECs, and hillock cells. Hyperoxia exposure and treatment with dexamethasone caused significant cellular transcriptional changes and highlighted biological pathways, both known and novel, with distinct findings based on sex as a biological variable. Findings were validated in an independent dataset from human BPD lung samples. Infant BAL-derived human lung organoids represent a cutting-edge model that bridges a critical gap in BPD research. They combine the advantages of being patient-specific and capturing developmental lung biology, with the experimental flexibility of an <em>in vitro</em> system.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 104057"},"PeriodicalIF":11.9,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146072061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Are glutathionylated aldehyde reductases the missing piece of the “catecholaldehyde hypothesis” in Parkinson's disease? A medical hypothesis concerning the detoxification of 4-hydroxynonenal (HNE) and 3,4-dihydroxyphenylacetaldehyde (DOPAL)","authors":"Rossella Rotondo ,&nbsp;Marta Russo ,&nbsp;Federico Iacovelli ,&nbsp;Valeria Calabrese ,&nbsp;Antonio de Iure ,&nbsp;Maria Gaglione ,&nbsp;Lorenza Leonardi ,&nbsp;Gabriella Cocorocchia ,&nbsp;Fabrizio Stocchi ,&nbsp;Vilberto Stocchi ,&nbsp;Maria Francesca de Pandis ,&nbsp;Barbara Picconi","doi":"10.1016/j.redox.2026.104060","DOIUrl":"10.1016/j.redox.2026.104060","url":null,"abstract":"<div><div>The autotoxicity of the monoamine oxidase (MAO) reaction product 3,4-dihydroxyphenylacetaldehyde (DOPAL) is central to the “<em>catecholaldehyde hypothesis”</em>, which posits that interactions between DOPAL and the protein α-synuclein contribute to the degeneration of catecholaminergic neurons in Parkinson's disease (PD). Dopamine (DA) can undergo spontaneous or enzymatic oxidation, generating dopamine-quinone (DA-Q) and DOPAL, respectively. While growing evidence highlights the quinonization of numerous proteins in catecholaminergic cells due to the high reactivity of DA-Q, the electrophilic properties of DOPAL and its quinone derivative (DOPAL-quinone, DOPAL-Q) have received less attention, along with potential detoxification pathways.</div><div>Here, we propose a refinement of the “<em>catecholaldehyde hypothesis”</em> by extending the detoxification machinery described for 3-glutathionyl-4-hydroxynonenal (GS-HNE) to the formation of glutathionylated DOPAL adducts. Conjugation of DOPAL-Q with glutathione (GSH) would generate 5-S-glutathionyl-3,4-dihydroxyphenylacetaldehyde (GS-DOPAL). Analogous to GS-HNE, the aldehyde group of GS-DOPAL could be reduced to 5-S-glutathionyl-3,4-dihydroxyphenylethanol (GS-DOPET) by glutathione-dependent aldehyde reductases such as aldose reductase (AKR1B1) and carbonyl reductase 1 (CBR1). Conversely, oxidation of the phenolic hydroxyl groups by CBR1 to yield 5-S-glutathionyl-3,4-dioxophenylacetaldehyde (GS-DOPAL-Q) may also occur. We suggest that the excretion of such GS-adducts via glutathione-electrophile transporters could open new perspectives for identifying early biomarkers of PD and for evaluating the disease-modifying potential of MAO inhibitors.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 104060"},"PeriodicalIF":11.9,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146072059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DMNQ induces ferroptosis and augments the efficacy of anti-PD-L1 immunotherapy in gastric cancer via the STAT3/SLC1A4 axis to mediate cysteine metabolism reprogramming","authors":"Wenshuai Zhu ,&nbsp;He Qi ,&nbsp;Fubo Jing ,&nbsp;Yuxuan Shi ,&nbsp;Yuanxin Xing ,&nbsp;Xiaoli Ma ,&nbsp;Bin Ning ,&nbsp;Yunshan Wang ,&nbsp;Yanfei Jia","doi":"10.1016/j.redox.2026.104055","DOIUrl":"10.1016/j.redox.2026.104055","url":null,"abstract":"<div><div>Ferroptosis plays an essential role in tumor progression. Therapeutic agents targeting ferroptosis emerge as a novel strategy for cancer treatment. Abnormal amino acid metabolism can control ferroptosis sensitivity in cancer cells, and lead to the deficiency or accumulation of specific products in the tumor microenvironment (TME). Here, we demonstrated that 2,3-dimethoxy-1,4-naphthoquinone (DMNQ) induced growth inhibition in gastric cancer cell lines, primary gastric cancer mouse models, and patient-derived tumor organoids. DMNQ exerted ferroptosis inducing effects by inhibiting STAT3 phosphorylation and transcriptional activity. Importantly, the STAT3/SLC1A4 axis regulated cysteine uptake, tumor killing by T cells and the efficacy of anti-PD-L1 immunotherapy. Collectively, our findings revealed a critical mechanism by which DMNQ exerts a significant anti-cancer role in gastric cancer through increasing ferroptosis to enhance cancer immunotherapy and may provide a novel therapeutic strategy for gastric cancer.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 104055"},"PeriodicalIF":11.9,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146048384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"XPR1 downregulation inhibits hepatocellular carcinoma progression by suppressing serine metabolism","authors":"Zi-qiang Liao ,&nbsp;Ze-ning Chen ,&nbsp;Yang-feng Lv ,&nbsp;Yuan-yuan Zhang ,&nbsp;Zhi-xing Liu ,&nbsp;Zhi-qiang Deng ,&nbsp;Qing-rong Liang ,&nbsp;Chun-bo Zhang ,&nbsp;Qun Tang","doi":"10.1016/j.redox.2026.104053","DOIUrl":"10.1016/j.redox.2026.104053","url":null,"abstract":"<div><div>Xenotropic and polytropic retrovirus receptor 1 (XPR1) is highly expressed in various tumors and is associated with poor clinical prognosis, making it a proposed therapeutic target for cancer. However, the mechanism of XPR1 in tumorigenesis, particularly in hepatocellular carcinoma (HCC), remains unclear. Emerging evidence suggests that the knockdown of XPR1 in HCC cells leads to redox imbalance and mitochondrial damage. In this study, we aimed to investigate the molecular mechanisms and novel biological functions of XPR1 in HCC. Our findings revealed that XPR1 knockdown downregulated PHGDH expression, resulting in reduced serine biosynthesis, compromised redox homeostasis, exacerbated DNA damage, and pronounced mitochondrial fragmentation. Importantly, we identified MNX1 as a transcription factor of PHGDH. Restoration of MNX1 or PHGDH expression in XPR1-knockdown HCC cells effectively restored redox homeostasis and rescued tumor progression-associated functions. Moreover, in HCC cells in which XPR1 was knocked down, the re-expression of PHGDH effectively restored the intracellular serine level and tumorigenic capacity in vivo. Taken together, the results of our study demonstrate that XPR1 knockdown in HCC disrupts MNX1-mediated regulation of PHGDH expression, impairing serine metabolism and inducing redox imbalance, ultimately suppressing HCC progression. These findings suggest that XPR1 may serve as a therapeutic target for HCC.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 104053"},"PeriodicalIF":11.9,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146048385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UFMylation deficiency in hepatocytes activates the KEAP1-NRF2 pathway and contributes to hepatocarcinogenesis","authors":"Qian Liang ,&nbsp;Shiwen Xu ,&nbsp;Yaoyao Fang ,&nbsp;Xue Wang ,&nbsp;Yang Xiao ,&nbsp;Yiwen Wang ,&nbsp;Shujuan Li ,&nbsp;Qifan Guo ,&nbsp;Yu Cao ,&nbsp;Ying Cao ,&nbsp;Chao Liu ,&nbsp;Yuqin Zhao ,&nbsp;Yan Luo ,&nbsp;Anqi Wu ,&nbsp;Miao Wang ,&nbsp;Junping Shi ,&nbsp;Guoqing Li ,&nbsp;Yu-Sheng Cong","doi":"10.1016/j.redox.2026.104046","DOIUrl":"10.1016/j.redox.2026.104046","url":null,"abstract":"<div><div>The Kelch-like ECH-associated protein 1 (KEAP1) - Nuclear factor erythroid 2-related factor 2 (NRF2) pathway plays a central role in maintaining cellular redox balance, aberrant activation of the KEAP1-NRF2 pathway is involved in a variety of human malignant tumors including hepatocellular carcinoma. However, the underlying mechanisms remain unclear. UFMylation is a type of ubiquitin-like modifications with important biological functions, its deficiency is implicated in several pathogenesis. In this study, we show that hepatocyte specific <em>Ufl1</em> knockout in mice results in several hepatic pathological alterations and promotes the development of diethylnitrosamine (DEN)-induced hepatocarcinogenesis. Furthermore, we identified KEAP1 as an UFMylation substrate, and deficiency in UFMylation modification resulted in ubiquitin-mediated degradation of KEAP1, and subsequent nuclear accumulation of NRF2, and activation of the KEAP1-NRF2 pathway. Consistently, we found that UFL1 expression is decreased and positively correlated with the level of KEAP1 in liver cancer samples. Our results suggest that UFL1 plays an important role in liver pathophysiology, in part by regulating the KEAP1-NRF2 pathway, thus provides novel insights into the molecular basis of hepatocarcinogenesis.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 104046"},"PeriodicalIF":11.9,"publicationDate":"2026-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146048386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Dual Roles of Natural Cannabidiol in Combating Oxidative Stress and Inflammation: A Potential Intestinal Guardian","authors":"Biguang Lv, Jieyi He, Sha Zhan, Ke Jin, Xinyu Lei, Xuan Cheng, Zonghao Lv, Fengming Chen, Yuying Li, Jun Lu, Qian Lin","doi":"10.1016/j.redox.2026.104051","DOIUrl":"https://doi.org/10.1016/j.redox.2026.104051","url":null,"abstract":"Cannabidiol (CBD), a non-psychoactive and non-addictive phytocannabinoid derived from <ce:italic>Cannabis sativa</ce:italic> L., has attracted increasing attention for its therapeutic potential in intestinal diseases. Accumulating evidence indicates that CBD exerts prominent antioxidant and anti-inflammatory effects within the gastrointestinal tract. Oxidative stress and redox imbalance are key drivers of epithelial barrier dysfunction, chronic inflammation, and disease progression in disorders such as inflammatory bowel disease (IBD) and colorectal cancer (CRC). This review focuses on the redox-related mechanisms underlying CBD’s intestinal protective actions, highlighting its ability to regulate reactive oxygen species (ROS) production, activate the Nrf2–Keap1 antioxidant pathway, and modulate redox-sensitive inflammatory signaling, including NF-κB and the NLRP3 inflammasome. In parallel, CBD engages the endocannabinoid system (ECS) and related receptors to preserve epithelial barrier integrity, regulate gut microbiota composition, and modulate intestinal oxidative stress and inflammation. We further discuss emerging evidence linking CBD’s regulation in the gut to systemic effects along the gut–organ axis, including the gut–brain and gut–liver axes. Overall, this review synthesizes current evidence on how CBD integrates redox modulation, inflammation control, and intestinal barrier protection, providing a mechanistic framework for its potential application in intestinal disease and health.","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"274 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2026-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146048387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myo1f regulates monocyte adhesion and contributes to atherosclerosis via MRTFA-dependent ITGB2 expression","authors":"Yifei Lv,&nbsp;Xiaomin Jiang,&nbsp;Yu Chang,&nbsp;Rongrong Huang,&nbsp;Yunwei Chen,&nbsp;Yunfei Deng,&nbsp;Yue Gu,&nbsp;Shaoliang Chen,&nbsp;Linlin Zhu","doi":"10.1016/j.redox.2026.104049","DOIUrl":"10.1016/j.redox.2026.104049","url":null,"abstract":"<div><h3>Background</h3><div>Monocyte adhesion to vascular endothelial cells is a critical step in the pathogenesis of atherosclerosis. While unconventional myosins are known to participate in various cellular activities, their specific role in monocyte-endothelium adhesion remains unclear.In the present study, we investigated the effects of Myosin IF (Myo1f), a class I unconventional myosin, on atherosclerosis and its underlying mechanisms.</div></div><div><h3>Methods</h3><div>A high-cholesterol diet was administered to apolipoprotein E-KO (<em>Apoe</em>^{<em>−/−</em>}) mice to establish an atherosclerosis model, which was further combined with Myo1f knockout to investigate the specific role of Myo1f in atherosclerosis development. Bone marrow transplantation was conducted to assess the significance of Myo1f in myeloid cells related to atherosclerosis. Peripheral blood mononuclear cells (PBMCs) from patients with non-coronary artery disease (non-CAD) and coronary artery disease (CAD) were isolated to examine the correlation between Myo1f and human atherosclerosis. Co-immunoprecipitation mass spectrometry analysis was performed to identify molecules associated with Myo1f, which were subsequently validated and mechanistically investigated through both in vivo and in vitro experiments. Additionally, potential therapeutic drugs for atherosclerosis were explored using the <em>Apoe</em>^{<em>−/−</em>} mouse model.</div></div><div><h3>Results</h3><div>Myo1f expression was found to be significantly increased in PBMCs of patients with coronary artery disease. Moreover, Myo1f-deficient mice exhibited a notable reduction in atherosclerotic plaque area and lipid deposition compared to <em>Apoe</em>^{<em>−/−</em>} mice. Notably, monocyte Myo1f deletion obviously reduced its integrin β2 (ITGB2) expression, consequently impeding the adhesion of monocytes to vascular endothelial cells. Mechanistically, Myo1f promoted actin polymerization by recruiting epithelial protein lost in neoplasm (EPLIN) and depolymerization of G-actin/myocardin-related transcription factor A (MRTFA), leading to the nuclear translocation of MRTFA and upregulation of ITGB2 transcriptional expression. Treatment with CCG-1423, a MRTFA inhibitor, resulted in reduced atherosclerotic lesions in <em>Apoe</em>^{<em>−/−</em>} mice.</div></div><div><h3>Conclusions</h3><div>Our data indicate that Myo1f regulates monocyte adhesion and contributes to the pathogenesis of atherosclerosis by recruiting EPLINα, which stabilizes F-actin. This stabilization enhances MRTFA nuclear translocation, thereby promoting ITGB2 transcription.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 104049"},"PeriodicalIF":11.9,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146033550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRF2: Master regulator of cellular homeostasis and therapeutic vulnerability in cancer","authors":"Wei-tai Chen ,&nbsp;Nicholas W. McKee ,&nbsp;Damaris Kuhnell ,&nbsp;Matthew Dodson","doi":"10.1016/j.redox.2026.104050","DOIUrl":"10.1016/j.redox.2026.104050","url":null,"abstract":"<div><div>The transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is best known for its regulation of the antioxidant response. However, its mediation of other pathways, including key aspects of metabolic and protein homeostasis, has continued to emerge. Accompanying this emergence is an evolved understanding that NRF2 induction across different disease contexts can be beneficial or detrimental depending on the length of activation. This has played an important role in progressing the field forward, as inducing NRF2 is not always the best course of action, and inhibition has gained traction as a viable strategy for treating cancer and other pathologies where NRF2 is chronically active. Despite its rapid growth and a wealth of experimental promise, a persistent shortcoming in the field is a lack of NRF2-specific therapeutics used in clinic. Thus, despite recent advances, there is still room for progress in translating experimental evidence into therapeutic reality. In this review, we will provide a summary of NRF2 regulation and an update on its expanded network of downstream transcriptional programs. We will also discuss targeting NRF2 in disease, focusing on intervention versus prevention depending on the pathological context. Finally, we will briefly highlight current limitations in the field, as well as ongoing approaches that show promise for finally targeting this critical cascade in patient populations.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 104050"},"PeriodicalIF":11.9,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146033556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Redox biomarkers in dietary interventions and nutritional observation studies - From new insights to old problems” [Redox Biol. 41 (2021) 101922]","authors":"Thorsten Henning ,&nbsp;Daniela Weber","doi":"10.1016/j.redox.2026.104028","DOIUrl":"10.1016/j.redox.2026.104028","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 104028"},"PeriodicalIF":11.9,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146042500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of exercise training on nitric oxide pathways and their physiological effects","authors":"Jonas Benjamim ,&nbsp;Stephen J. Bailey ,&nbsp;Leonardo da Silva Gonçalves ,&nbsp;Mia Burleigh ,&nbsp;Mario Siervo ,&nbsp;Andrew R. Coggan ,&nbsp;Raúl Bescos","doi":"10.1016/j.redox.2026.104041","DOIUrl":"10.1016/j.redox.2026.104041","url":null,"abstract":"<div><div>Nitric oxide (NO) is a critical signalling molecule in cardiovascular, metabolic, and muscular function. Endogenous NO production occurs via two primary metabolic pathways: 1) the classical nitric oxide synthases (NOS) pathway, and 2) the alternative (nitrate–nitrite–NO) pathway, in which inorganic nitrate (NO₃⁻) is sequentially reduced to nitrite (NO₂⁻) and other NO intermediates (e.g., S-nitrosothiol). The latter pathway relies heavily on the oral microbiota, which catalyze the two-electron partial reduction of NO₃⁻ to NO₂⁻, which is influenced by oral physiology, microbial composition and salivary flow. While the role of exercise training in enhancing NOS-derived NO is well established, emerging evidence suggests that it may also augment NO bioavailability through the NO₃⁻–NO₂^-–NO pathway. Furthermore, exercise training may influence the composition and functionality of oral microbiota, thereby indirectly modulating NO metabolism and oral health. However, the synergistic effects of exercise and oral microbiota on NO production remain underexplored. This review synthesises current evidence on how physical exercise may modulate both NO pathways and discusses the broader physiological implications.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 104041"},"PeriodicalIF":11.9,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146033551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}