Journal of physiology and biochemistry最新文献

{"title":"Lipoxin A4 activates Nrf2 expression and mitigates hyperglycaemia-induced impairment of myogenesis and rescues damage to mitochondria.","authors":"Akash Mitra, Deepika Bhat K, Joel Rimson Pinto, Samanwita Mandal, Undurti Narasimha Das, Bipasha Bose, Sudheer Shenoy P","doi":"10.1007/s13105-026-01166-2","DOIUrl":"10.1007/s13105-026-01166-2","url":null,"abstract":"<p><p>High glucose toxicity or hyperglycaemia manifests through various downstream processes, one of which is the elevation of oxidative stress. One of the consequences of increased reactive oxygen species production is mitochondrial damage, both metabolically and structurally. Arachidonic acid (AA) has been shown to salvage mitochondrial dysfunction in skeletal muscles. In this study, we explore the effects of lipoxin A4 (LXA4), a downstream anti-inflammatory metabolite of arachidonic acid, on mitigating hyperglycaemia-induced oxidative stress at the molecular level. We observed that LXA4 could substantially inhibit ROS production and restore Nrf2 expression (by 14%). Additionally, lipoxin A4 treatment was able to restore the mitochondrial potential and prevent mitochondrial fragmentation. Finally, due to the rescue of mitochondrial homeostasis and energetics, the process of myogenesis, an energy-extensive phenomenon, was also restored by the lipid treatment as evident from the differentiation parameters like myotube diameter and myonuclei fusion index, and the expression of MyoD, which drives the transition of myoblasts from proliferation to differentiation.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147326438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in circulating bile acid levels during cold exposure are associated with brown adipose tissue in humans: a secondary analysis from the ACTIBATE study.","authors":"Lucas Jurado-Fasoli, Borja Martinez-Tellez, Isabelle Kohler, Jonatan R Ruiz, Francisco J Osuna-Prieto","doi":"10.1007/s13105-026-01155-5","DOIUrl":"10.1007/s13105-026-01155-5","url":null,"abstract":"<p><p>Cold exposure activates brown adipose tissue (BAT), a therapeutic target to mitigate cardiometabolic diseases. Emerging evidence suggests that bile acids may influence BAT activity through metabolic and endocrine signaling pathways. Characterizing changes in circulating bile acids during cold exposure may uncover new pathways to improve metabolic health in humans. We analysed 56 young (21.7 ± 2.3 years old), sedentary adults (43 women, 77%) from the ACTIBATE cohort (NCT02365129) before the intervention in whom plasma samples were available for bile acid analyses. Eighteen plasma bile acid species were analyzed using liquid chromatography-tandem mass spectrometry before (i.e., baseline), 60, and 120 min during a personalized cooling protocol. BAT volume, activity, and radiodensity were assessed via 18F-fluorodeoxyglucose positron emission tomography-computed tomography scan (18F-FDG PET-CT) at the end of the cooling protocol. During the 2-hour cold exposure, plasma levels of total, secondary, and conjugated bile acids decreased by 24–30% (all P < 0.001). In normal-weight participants, most reductions remained significant after adjustment for PET-CT time, and glycolithocholic acid (GLCA) showed consistent positive associations with BAT volume and glucose uptake, as well as an inverse association with radiodensity (|r|≤0.41, adj. FDR ≤ 0.25; R ≤ 0.34, P ≤ 0.038 in adjusted regression models). In participants with overweight or obesity, most bile-acid changes lost statistical significance after adjustment for PET-CT time, although lithocholic acid and its sulfated derivative remained positively correlated with BAT radiodensity (|r|≤0.53; adj. FDR ≤ 0.25). Acute cold exposure is associated with changes in circulating bile acids in humans, with patterns differing by body-weight status. In normal-weight individuals, GLCA displayed consistent associations with BAT volume and glucose uptake, suggesting a possible link between bile acid and BAT activation. Further studies are needed to confirm these observations and to clarify the physiological relevance of bile acid signaling in human thermogenic adaptation.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12950022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147317484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic syndrome necroptosis: disease implications and therapeutic targeting.","authors":"Jiaenli Bolati, Ahequeli Gemingnuer, Fang Lu, Yueqi Yan, Donghua Yu, Chunmiao Yu","doi":"10.1007/s13105-026-01161-7","DOIUrl":"10.1007/s13105-026-01161-7","url":null,"abstract":"<p><p>Necroptosis is a regulated form of cell death characterized by receptor-interacting protein kinase (RIPK) activation, leading to necrosome formation and subsequent membrane rupture. Increasing evidence indicates that necroptosis contributes to metabolic syndrome (MetS) by promoting tissue inflammation, insulin resistance, and metabolic dysfunction. The molecular mechanisms underlying necroptosis in MetS primarily involve activation of the RIPK1-RIPK3-MLKL axis, particularly in metabolically active tissues such as skeletal muscle, liver, adipose tissue, and pancreatic β-cells. Although numerous experimental studies have linked necroptosis to metabolic inflammation and organ injury, a systematic synthesis of its mechanistic roles, biomarker relevance, and translational potential in MetS remains limited. This review summarizes current evidence on the molecular regulation of necroptosis in MetS, its involvement in disease progression across multiple organs, and emerging diagnostic, prognostic, and theragnostic biomarkers. In addition, this review discusses therapeutic strategies targeting necroptosis and critically evaluates their translational challenges. By integrating mechanistic and translational perspectives, this review aims to provide a balanced framework for understanding the role of necroptosis in MetS and to highlight key knowledge gaps that warrant further investigation.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147317516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Irisin/PGC-1-α improves acute kidney injury by enhancing autophagy and regulating lipid metabolism.","authors":"Jinrun Han, Hailin Yang, Fangning Liu, Xuheng Liu, Xiaoping Zhang, Jun Yang","doi":"10.1007/s13105-026-01159-1","DOIUrl":"10.1007/s13105-026-01159-1","url":null,"abstract":"<p><p>Acute kidney injury (AKI) is a critical clinical condition characterized by rapid loss of renal function and high morbidity. Irisin, a muscle-derived myokine, has been reported to exert protective effects in multiple tissues; however, its role in AKI remains largely unexplored. This study aimed to elucidate the renoprotective effects of irisin and its underlying mechanisms, with a particular focus on PGC-1α activation and autophagy regulation. Male C57BL/6 mice were subjected to lipopolysaccharide (LPS)–induced AKI and treated intravenously with irisin (10 mg/kg). Renal function, histopathological alterations, inflammatory markers, and apoptosis were assessed. In vitro, HK-2 cells were exposed to irisin, PGC-1α-specific siRNA, or the autophagy inhibitor chloroquine (CQ). Autophagic flux, lipid metabolism, mitochondrial function, and oxidative stress were subsequently evaluated. Irisin treatment markedly improved renal function in AKI mice by lowering serum creatinine and blood urea nitrogen levels, attenuating tubular injury, and suppressing inflammation and apoptosis. In HK-2 cells, irisin upregulated PGC-1α expression and enhanced autophagic activity, effects that were abolished by PGC-1α knockdown or CQ treatment. Additionally, irisin promoted lipid catabolism, reduced intracellular ROS accumulation, stabilized mitochondrial membrane potential, and protected cells from LPS-induced injury. Irisin alleviates AKI by activating PGC-1α–mediated autophagy, thereby mitigating inflammation, lipid accumulation, oxidative stress, and cellular damage. These findings highlight irisin as a potential therapeutic candidate for preventing or treating AKI.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147307156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined functional lipids modulate lipid metabolism and attenuate metabolic dysregulation in a rat model of cafeteria diet.","authors":"Candela L Suppo, Gisela N Kuhn, Jimena V Lavandera, Claudio A Bernal, Ana C Fariña","doi":"10.1007/s13105-026-01157-3","DOIUrl":"10.1007/s13105-026-01157-3","url":null,"abstract":"<p><p>Functional lipids (FL), including n-3 polyunsaturated fatty acids (PUFA) and conjugated linoleic acid (CLA), modulate lipid composition and gene expression, potentially mitigating lipid accumulation and related metabolic disorders. This study investigated whether the combination of FL (cFL), derived from virgin flaxseed oil (vFO) and CLA, prevent cafeteria (CAF) diet-induced metabolic dysfunctions, under the hypothesis that they could exert beneficial synergetic effects. Male Wistar rats were fed control diet (C), CAF, or CAF enriched with FL (vFO, CLA, or both -cFL-) for 10 weeks. Nutritional parameters, body composition, serum and hepatic triacylglycerol (TAG), tissue fatty acid (FA) profile, enzymatic activities, and genes involved in lipid metabolism were evaluated. CAF diet increased energy intake (EI), fat depots and body weight. CLA and cFL attenuated body weight and adipose tissue (AT) gain, despite similar EI. In CAF, hepatic TAG increased whereas serum TAG levels decreased, likely reflecting enhanced lipoprotein lipase (LPL) activity together with reduced TAG secretion rate (TAG-SR) and microsomal triglyceride transfer protein (MTTP) expression. vFO and cFL groups modulated FA composition, increasing n-3 PUFA and reducing n-6 PUFA. CLA and cFL groups decreased hepatic TAG with enhanced β-oxidation. Nutrigenomic analysis revealed changes in several genes, indicating transcriptional regulation of lipid metabolism in FL-enriched groups. In summary, cFL improved nutritional parameters and prevented hepatic TAG accumulation by enhancing lipid oxidation and TAG-SR, linked to transcriptional and post-transcriptional regulation of lipid metabolism genes. cFL exerted synergistic effects, improving metabolic profile and mitigating CAF-induced alterations, supporting their potential application in precision nutrition strategies.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147290301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive analysis and therapeutic implications of prognostic value of circadian rhythm genes in hepatocellular carcinoma.","authors":"Jichun Sun, Jiaxing Hou, Hongbo Xu, Zhiqiang Li, Zhen Deng, Zhi Yang, Wuqing Cao, Junning Hou, Xiaoxin Jin","doi":"10.1007/s13105-026-01150-w","DOIUrl":"10.1007/s13105-026-01150-w","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a prevalent and deadly malignancy, with a significant global impact. In this study, the role of circadian rhythm genes in HCC prognosis was investigated. Publicly available gene expression datasets from TCGA and GEO were analyzed to identify differentially expressed circadian genes. Weighted gene co-expression network analysis (WGCNA) was performed to construct circadian gene modules, which were then correlated with clinical traits. Unsupervised clustering identified two distinct HCC subtypes based on circadian gene expression profiles, with significant differences in overall survival. Functional enrichment analysis revealed that these subtypes are associated with distinct metabolic and immune-related pathways. A prognostic model was constructed using LASSO regression, incorporating key circadian genes that stratified patients into high- and low-risk groups. The model was validated in independent cohorts and demonstrated robust predictive power. Additionally, a nomogram integrating circadian gene expression with clinical factors was developed to enhance individualized prognostic predictions. Further validation of key genes, particularly GPT (glutamate pyruvate transaminase), highlighted its potential as a tumor suppressor and therapeutic target within HCC. Experimental validation using qRT-PCR and IHC confirmed elevated expression levels of GHR, IGFBP3, and GPT in tumor tissues, underscoring their clinical relevance and prognostic value. These findings underscore the importance of circadian rhythm disruptions in HCC progression and suggest potential therapeutic targets for improving patient outcomes.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147307090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Concurrent initiation of treadmill exercise protects against angiotensin II-induced renal injury by modulating oxidative stress and autophagy in mice.","authors":"Kyung-Wan Baek, Jong-Hwa Won, Ying-Ying Xiang, Dong Kyun Woo, Yoonjung Park, Ji-Seok Kim","doi":"10.1007/s13105-026-01158-2","DOIUrl":"10.1007/s13105-026-01158-2","url":null,"abstract":"<p><p>Angiotensin II (AngII) promotes oxidative stress, inflammation, and fibrosis, contributing to progressive renal injury. Parallel 3- and 4-week experiments were conducted in male C57BL/6 mice (n = 48). Mice received daily subcutaneous injections of AngII (1.4 mg/kg/day) or vehicle (Veh), and were assigned to one of four groups at each time point: Veh, AngII, AngII with low-intensity exercise (LIE) (AngII + LIE; 75 min/day at 12 m/min), or AngII with high-intensity exercise (HIE) (AngII + HIE; 50 min/day at 18 m/min). Renal injury was assessed via histology, Sirius Red staining for fibrosis, and molecular analyses of oxidative stress, podocyte integrity, inflammation (transforming growth factor [TGF-β] and inducible nitric oxide synthase [iNOS]), apoptosis (cleaved caspase-3 and p-phosphorylated c-Jun N-terminal kinase [JNK]), and autophagy (microtubule-associated protein 1 light chain 3 beta [LC3B], sequestosome [p62], autophagy-related proteins [ATG]3, 5, and 7)-related protein and gene expression. AngII triggered time-dependent renal pathology, with early molecular apoptotic stress responses evident by week 3 and substantially more pronounced histological and molecular damage by week 4 (p < 0.05). The 4-week AngII group exhibited significantly increased fibrosis (~ 2-fold vs. Veh, p < 0.01), elevated TGF-β and iNOS expression, and disrupted autophagic flux, including increased LC3-II/I ratio and ATG expression, alongside decreased p62 levels. These alterations were markedly improved in AngII + HIE mice (p < 0.01), whereas AngII + LIE showed partial effects. These findings suggest that exercise initiated during the early phase of hypertensive stress effectively attenuates the progression of renal oxidative damage, inflammation, apoptosis, and dysregulated autophagy, thereby slowing the progression of AngII-induced kidney injury.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":"13"},"PeriodicalIF":5.1,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146220073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From molecular mechanisms to nutritional applications: protein and polyphenol interventions in sarcopenia.","authors":"Patricia Aragón-Espinosa, Patricia Pérez-Matute, Catherine Bompart, Marine Gueugneau, Frederic Capel, Jose M Arbones-Mainar, Saioa Gomez-Zorita, Anna Mas-Capdevila, Xavier Escoté, Montserrat Pinent, Anna Ardévol","doi":"10.1007/s13105-026-01154-6","DOIUrl":"10.1007/s13105-026-01154-6","url":null,"abstract":"<p><p>Sarcopenia, the progressive loss of skeletal muscle mass and function, represents a major public health concern due to its impact on mobility, independence, and quality of life, especially in oldadults. Current treatment strategies primarily rely on resistance training and nutritional support, with particular emphasis on adequate protein intake to stimulate muscle protein synthesis. In this review, we provide an overview of the pathophysiology of sarcopenia, with a focus on the molecular mechanisms underlying muscle atrophy and dysfunction. We explore the role of dietary protein as a cornerstone of sarcopenia management, highlighting current evidence on optimal protein sources and intake strategies. In addition, we examine other nutritional interventions, placing special emphasis on polyphenols, naturally occurring compounds known for their antioxidant and anti-inflammatory properties, which have shown promise in modulating pathways relevant to muscle preservation. Vitamin D and other nutritional supplements are also discussed in the context of their potential to support muscle health. Finally, we address emerging trends in the field, including targeting microbiota. By integrating current findings, this narrative review aims to provide a compilation of the evidence-based nutritional interventions for the prevention and management of sarcopenia.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":"12"},"PeriodicalIF":5.1,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12909418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146201928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resveratrol and dexamethasone have cell-specific effects on the circadian clock but not on the rhythm of mitochondrial function in the fetal heart.","authors":"Dmytro Semenovykh, Kateryna Semenovykh, Martin Sládek, Alena Sumová","doi":"10.1007/s13105-026-01152-8","DOIUrl":"10.1007/s13105-026-01152-8","url":null,"abstract":"<p><p>Proper development of the heart during the fetal period is a prerequisite for health in later life. It was shown that maternal supplementation with stilbenoid resveratrol (RES) is beneficial for cardiovascular function. Synthetic glucocorticoid dexamethasone (DEX) is commonly used in the prenatal treatment of respiratory distress syndrome. RES affects the circadian clock in various tissues but its effect on the fetal heart has not been studied. We hypothetized that RES may affect the the circadian clock via modulation of the glucocorticoid signaling and/or mitochondrial function. Therefore, we tested the effects of different concentrations of RES and synthetic glucocorticoid dexamethasone (DEX) on the circadian clock, energy metabolism and mitochondrial function in fetal cardiomyocytes (CMCs) and cardiac fibroblasts (FBs). We found that RES affects the clock in both CMCs and FBs by increasing the stability of the clock protein PER2. In CMCs, the effect was mediated via the adenylyl cyclase signaling pathway. RES modulated DEX-induced effects on the circadian clock in CMCs and FBs. We were able to detect a circadian rhythm in mitochondrial function in fetal heart cells, which was confirmed by ATP and resazurin assays as well as visualization of the mitochondrial network and reactive oxygen species (ROS). Interestingly, we found that both drugs shifted the phase of fetal heart clock, but had no effect on the phase of mitochondrial rhythmicity, indicating a possible uncoupling of circadian and mitochondrial rhythms in fetal CMCs and FBs. Overall, our data revealed fetal heart-specific effects of RES on the circadian clock through the stabilization of PER2 protein and its ability to modulate DEX-induced effects on the clock.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":"11"},"PeriodicalIF":5.1,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12909427/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146201943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise training reinforces the therapeutic efficacy of bone marrow-derived mesenchymal stem cell transplantation for ventricular ectopy and myocardial infarction injury.","authors":"Shirin Abazari, Seyed Abdollah Hashemvarzi, Kamal Ranjbar","doi":"10.1007/s13105-026-01148-4","DOIUrl":"10.1007/s13105-026-01148-4","url":null,"abstract":"<p><p>This study investigated the synergistic effect of early bone marrow-derived mesenchymal stem cells (BM-MSC) transplantation and endurance training on exercise-induced ventricular ectopy, myocardial infarction-induced injury and cardiac function in rats. 90 male Wistar rats (7-8 weeks) randomly distributed following groups, 1: Healthy control (HC, n = 15), 2: Sham (Sham, n = 15), 3 Myocardial infarction (MI, n = 15), 4: Myocardial infarction with BM-MSC transplantation (MI-SC, n = 15), 5: Myocardial infarction with Endurance training (MI-ET, n = 15) and 6: Myocardial infarction with Endurance training and BM-MSC transplantation (MI-ET + SC, n = 15). Myocardial infarction was induced by permanent obstruction of the cardiac left anterior descending artery. One day after MI induction, 1 × 10⁶ BM-MSC were injected via a caudal vein in MI-SC and MI-ET + SC groups, and training rat subjects were to run on a rodent treadmill for 10 weeks. BM-MSC alone decreased serum LDH, CK-MB, left ventricular Bax, and infarction size, and promoted serum IL-10, cardiac function and exercise capacities. These effects would be stronger if cell therapy was combined with exercise training. Cell therapy insignificantly decreased TNF-α and promoted left ventricular Bcl-2, but cell therapy with exercise training significantly reduced TNF-α and promoted Bcl-2. Despite the greater reduction of cardiac arrhythmia after exercise in the MI-ET + SC group, there was no significant difference between the treatment groups. The results of this study showed that exercise training and BM-MSC transplantation synergistically promoted myocardial infarction-induced injury healing and reduced ventricular ectopy after exercise in myocardial infarction rats via inflammation and apoptosis reduction.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":"10"},"PeriodicalIF":5.1,"publicationDate":"2026-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146194763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}