Journal of physiology and biochemistry最新文献_第9页

Mfn1-mediated imbalanced mitochondrial dynamics promotes ovarian cancer stemness by inducing metabolic reprogramming. mfn1介导的线粒体动力学失衡通过诱导代谢重编程促进卵巢癌的发生。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-18 DOI: 10.1007/s13105-026-01172-4

Rahail Ashraf, Kalpana Tankay, Manita Raina, Athira, Sanjay Kumar

{"title":"Mfn1-mediated imbalanced mitochondrial dynamics promotes ovarian cancer stemness by inducing metabolic reprogramming.","authors":"Rahail Ashraf, Kalpana Tankay, Manita Raina, Athira, Sanjay Kumar","doi":"10.1007/s13105-026-01172-4","DOIUrl":"10.1007/s13105-026-01172-4","url":null,"abstract":"Ovarian cancer (OC) is the leading cause of death from reproductive system cancer among women worldwide. Ovarian cancer stem cells (OCSCs) are critically involved in metastasis, tumor recurrence, and chemoresistance, and are a significant bottleneck in the treatment. Several studies demonstrated metabolic rewiring and altered mitochondrial dynamics in CSCs. However, the role of Mfn1-mediated imbalanced mitochondrial dynamics in ovarian cancer stemness remains poorly understood. In this study, quantification of mtDNA indicates that CSCs have increased mitochondrial mass compared to the parental adherent cells. CD133+ enriched cells and cancer stem-like cells (spheroid cultured from OC cells) have higher Mfn1 expression and mitochondrial fusion activity. CSCs have increased oxidative phosphorylation (OXPHOS), ATP, and reduced ROS compared to the parental adherent cells. Disruption of mitochondrial dynamics by depletion of Mfn1 modulates the growth and size of spheroid formation and OC stemness. Seahorse analyzer analysis confirms the functional impact of Mfn1 knockdown on mitochondrial respiration. Overexpression of Mfn1 in SKOV-3 cells, which have a naturally low level of Mfn1, induces increased mitochondrial respiration. Furthermore, to elucidate the relationship between Mfn1 and OXPHOS complex activities and their role in OC stemness, we treated OC cells with 2-Deoxy-D-glucose (2DG), which induces OXPHOS and modulates the cancer stemness through Mfn1. During stemness acquisition, CSCs undergo Mfn1-mediated mitochondrial rearrangement, which could be a potential therapeutic strategy against ovarian cancer.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147474221","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}

引用次数: 0

Time-of-day-dependent effects of exercise on the hepatic clock and proteome in high-fat diet-fed mice. 运动对高脂肪饮食小鼠肝脏时钟和蛋白质组的时间依赖性影响。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-18 DOI: 10.1007/s13105-026-01168-0

Chunxiu Huang, Xiaodan Wang, Huanghao Zhou, JingFang Zhu, Yue Hu, Huijuan Wu, Xinru Yu, Cong Chen

{"title":"Time-of-day-dependent effects of exercise on the hepatic clock and proteome in high-fat diet-fed mice.","authors":"Chunxiu Huang, Xiaodan Wang, Huanghao Zhou, JingFang Zhu, Yue Hu, Huijuan Wu, Xinru Yu, Cong Chen","doi":"10.1007/s13105-026-01168-0","DOIUrl":"10.1007/s13105-026-01168-0","url":null,"abstract":"Circadian disruption exacerbates high-fat diet-induced metabolic disease, but whether the time-of-day exercise differentially remodels the hepatic clockwork and downstream metabolic circuits remains unclear. Male C57BL/6J mice were fed normal diet or a high-fat diet (HFD) and then underwent 8 weeks of morning or afternoon treadmill training. We evaluated glucose-lipid phenotypes and hepatic core clock proteins and conducted quantitative liver proteomics with trend-based clustering, followed by immunoblot validation. Both morning and afternoon exercise mitigated high-fat diet induced weight gain, improved glucose tolerance and insulin sensitivity, and reduced hepatic lipid accumulation relative to sedentary HFD controls, with greater benefits in the morning. HFD increased hepatic CLOCK, BMAL1, and CRY1 and suppressed REV-ERBα. Morning training preferentially normalized CLOCK, BMAL1, and CRY1, whereas afternoon training more prominently restored REV-ERBα. Proteomics identified two dynamic modules. Cluster 1 consists of proteins induced by diet and suppressed by exercise, including enzymes of bile acid synthesis such as CYP7A1 and components of protein N-glycosylation and endoplasmic reticulum proteostasis such as DAD1 and DPAGT1, which shifted toward control levels with exercise intervention. Cluster 7 comprises proteins reduced by diet and enhanced by exercise, including IDNK involved in nucleotide metabolism and ATP6V1G1 associated with autophagy and lysosomal function, with a stronger recovery after morning training. Immunoblotting corroborated these protein level changes. Exercise acts as a time-of-day-dependent modulator of the hepatic proteome. Morning exercise produced a more pronounced normalization of proteins implicated in bile acid metabolism, ER proteostasis, and autophagy-lysosome pathways, thereby nominating candidate mechanisms that may contribute to improved metabolic control under HFD.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147474249","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}

引用次数: 0

Correction: Molecular mechanisms of UCP1-independent thermogenesis: the role of futile cycles in energy dissipation. 校正：不依赖ucp1的产热的分子机制：无用循环在能量耗散中的作用。

IF 4.3 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-17 DOI: 10.1007/s13105-026-01149-3

Quanhao Sun, Xinyue Cui, Dong Yin, Juan Li, Jiarui Li, Likun Du

引用次数: 0

Aerobic exercise improve physical endurance and muscle function by ameliorating oxidative stress and modulating mitochondrial dynamics in aged skeletal muscle. 有氧运动通过改善氧化应激和调节老化骨骼肌的线粒体动力学来提高身体耐力和肌肉功能。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-17 DOI: 10.1007/s13105-026-01146-6

Fengting Zheng, Jiawei Zhou, Yangfan Cao, LuYi Lin, Wenxin Wang, Liang Zhang, Wei Li, Ting Li, Lifeng Wang

{"title":"Aerobic exercise improve physical endurance and muscle function by ameliorating oxidative stress and modulating mitochondrial dynamics in aged skeletal muscle.","authors":"Fengting Zheng, Jiawei Zhou, Yangfan Cao, LuYi Lin, Wenxin Wang, Liang Zhang, Wei Li, Ting Li, Lifeng Wang","doi":"10.1007/s13105-026-01146-6","DOIUrl":"10.1007/s13105-026-01146-6","url":null,"abstract":"Mitochondrial dysfunction is associated with the age-related decline in skeletal muscle mass and strength. Aerobic exercise upregulate Sestrins protein expression in skeletal muscle, which plays a key role in maintaining mitochondrial homeostasis. This study aimed to elucidate the role of aerobic exercise in regulating mitochondrial dynamics and oxidative stress in aging skeletal muscle. We randomly assigned male C57BL/6J mice into four groups: Young Control Group (YC), Young Aerobic Exercise Group (YA), Old Control Group (OC) and Old Aerobic Exercise Group (OA). We confirmed that aerobic exercise significantly enhanced grip strength and running capacity in aged mice compared to the OC group. The OC group exhibited significantly elevated MDA levels in skeletal muscle compared to the YC group, whereas aerobic exercise reduced MDA levels while increasing SOD and CAT activities in exercise group. Compared to the YC group, aging significantly reduced Sestrin1 protein expression, while Sestrin2 and Sestrin3 levels remained unaffected. Notably, aerobic exercise intervention significantly elevated Sestrin1 expression in OA group, compared to OC group, while no observable effects on Sestrin2/3 expression. Additionally Phospho-AMPK (Thr172), and PGC-1α were significantly increased in both the YA and OA groups. Aging also caused a marked decline in SDH activity and an increase in PGAM5 and OPA1 protein levels in the OC group. In addition, aerobic exercise improved SDH activity and augmented MFN2, OPA1 and PINK1 expression in YA and OA groups. In conclusion, aging induces oxidative stress accumulation and mitochondrial dysfunction in skeletal muscle, whereas 8-week of aerobic exercise mitigates these effects by upregulating Sestrin1 and its downstream targets, thus enhancing mitochondrial dynamics and function in aged mice.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147474143","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}

引用次数: 0

Glycocalyx degradation: exploring related mechanisms, pathophysiological significance, and therapeutic prospects. 糖萼降解：探讨相关机制、病理生理意义及治疗前景。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-09 DOI: 10.1007/s13105-026-01164-4

Yuwen Tian, Quan Zheng, Jiaxin Yin, Tian Liu, Wufeng Zhang, Yu Ban, Lisha Zheng, Wen Tang, Hongyan Kang

{"title":"Glycocalyx degradation: exploring related mechanisms, pathophysiological significance, and therapeutic prospects.","authors":"Yuwen Tian, Quan Zheng, Jiaxin Yin, Tian Liu, Wufeng Zhang, Yu Ban, Lisha Zheng, Wen Tang, Hongyan Kang","doi":"10.1007/s13105-026-01164-4","DOIUrl":"10.1007/s13105-026-01164-4","url":null,"abstract":"The glycocalyx is a fuzzy structure covering the luminal surface of vascular endothelial cells. Its name was first proposed by Bennett, derived from the Latin word meaning ‘sweet shell’. This was confirmed by Luft in 1966 through ruthenium red staining under electron microscopy. In recent years, the role of the glycocalyx in the pathophysiological processes of various diseases, such as cardiovascular diseases, chronic kidney disease, sepsis, COVID-19 infection, and diabetes, has gradually attracted widespread attention, and its importance has been increasingly recognized. In these acute and chronic clinical situations, the endothelium surface may lose syndecans, heparan sulfate (HS), and hyaluronan (HA), the primary constituents of the glycocalyx, a process involving multiple degrading enzymes. This review aims to start from the mechanisms of glycocalyx degradation, systematically elaborate on the factors related to degradation, enzymes involved in the degradation process, and signaling pathways. It also explores pharmacological drugs with the potential to reduce glycocalyx shedding, as found in current laboratory and clinical studies. In this review, it is expected to provide a reference for a deeper understanding of the role of glycocalyx in physiological and pathological processes and to offer new ideas and targets for the development of diagnostic, therapeutic, and preventive strategies for related diseases.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147390333","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}

引用次数: 0

Exercise attenuates high-fat diet-induced liver injury in mice via PPARα pathway and reduction of oxidative stress and inflammation. 运动可通过PPARα途径减轻小鼠高脂饮食引起的肝损伤，减少氧化应激和炎症。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-07 DOI: 10.1007/s13105-026-01167-1

Shunling Yuan, Jiaxin Liu, Jiyou Wu, Jianhui He, Liangwu Qiu

{"title":"Exercise attenuates high-fat diet-induced liver injury in mice via PPARα pathway and reduction of oxidative stress and inflammation.","authors":"Shunling Yuan, Jiaxin Liu, Jiyou Wu, Jianhui He, Liangwu Qiu","doi":"10.1007/s13105-026-01167-1","DOIUrl":"10.1007/s13105-026-01167-1","url":null,"abstract":"Fat acts as a “double-edged sword”—while serving as essential energy for the body, excessive long-term intake can lead to metabolic disorders and liver damage. With social progress and lifestyle changes, liver injury caused by chronic high-fat diet (HFD) has become a widespread and serious public health concern. In consideration of the unique role of exercise in lipid metabolism, we subjected mice to an HFD to investigate its effects on the livers of mice using RNA-Seq and other methods and comprehensively explore the mechanism of exercise’s regulatory effects on liver damage in HFD mice. Our results demonstrated that HFD could induce PPARα downregulation in the livers of mice, disrupt redox homeostasis, and trigger NF-κB-mediated inflammatory cascades, resulting in severe liver damage. Exercise can activate PPARα, inhibit NF-κB, reduce macrophage aggregation, as well as enhance HO-1 and SOD1 expression to regulate redox balance and inflammation. It is worth noting that HFD induces an increase in pro-oxidant activity and a decrease in antioxidant activity in the livers of mice, placing them in a state of oxidative stress. However, exercise simultaneously increases both pro-oxidant and antioxidant levels, alleviating oxidative stress. These results indicate that exercise can activate PPARα and regulate redox balance and inflammation, thereby protecting the livers of mice from the effects of HFD.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372962","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}

引用次数: 0

Luteolin ameliorates diabetic retinopathy through activation of the Nrf2/Keap1 and SIRT3/AMPK antioxidant axes and suppression of cGAS-STING and Wnt/β-catenin pathways in experimental rats. 实验大鼠木犀草素通过激活Nrf2/Keap1和SIRT3/AMPK抗氧化轴，抑制cGAS-STING和Wnt/β-catenin通路改善糖尿病视网膜病变。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-07 DOI: 10.1007/s13105-026-01170-6

Ruiwen Wang, Kangjie Guo, Jianchao Li

{"title":"Luteolin ameliorates diabetic retinopathy through activation of the Nrf2/Keap1 and SIRT3/AMPK antioxidant axes and suppression of cGAS-STING and Wnt/β-catenin pathways in experimental rats.","authors":"Ruiwen Wang, Kangjie Guo, Jianchao Li","doi":"10.1007/s13105-026-01170-6","DOIUrl":"10.1007/s13105-026-01170-6","url":null,"abstract":"Diabetic retinopathy (DR) is a sight-threatening complication of diabetes, which involves metabolic dysfunction, oxidative stress, inflammation, and angiogenesis. Luteolin, a dietary flavonoid, was examined for pleiotropic protective effects in streptozotocin-induced diabetic rats. Adult male Sprague-Dawley rats were assigned to five groups (n = 6): Control, Diabetic, Diabetic + Luteolin 50 mg kg⁻¹, Diabetic + Luteolin 100 mg kg⁻¹, and Diabetic + Metformin (300 mg kg⁻¹); treatments were given orally for eight weeks. Luteolin normalized fasting blood glucose (reduced by 48% at 100 mg/kg), restored circulating insulin (increased by 56.5%), reduced polyphagia (normalized to control levels), and prevented weight loss (maintaining 85% of initial body weight), indicating the recovery of systemic metabolism. Histology confirmed preservation of the total, inner, and outer retinal thickness, and a marked reduction in vascular leakage. Biochemically, luteolin lowered malondialdehyde, protein carbonyls, and advanced glycation end-products while elevating superoxide dismutase, catalase, and glutathione peroxidase, thus re-establishing the redox balance. Gene and protein analyses revealed synchronous pathway modulation: activation of the Nrf2/Keap1 antioxidant axis; upregulation of the mitochondrial SIRT3-AMPK-FOXO3 network and quality-control genes (Pink1, Park2, Sod2, Gpx4, and Hspa1a), suppression of the cGAS-STING-TBK1 innate immune cascade and downstream NF-κB-driven cytokines (Tnf, Il1b, Il6, Ifnb1); and inhibition of canonical Wnt/β-catenin signaling with reciprocal restoration of Gsk3b and downregulation of Vegfa. In conclusion, luteolin exerts comprehensive protective effects against DR by simultaneously correcting metabolic, oxidative, inflammatory, and angiogenic imbalances in diabetic rats. These findings highlight luteolin’s potential as an orally available and safe candidate for the prevention or delay of diabetic retinopathy progression.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372969","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}

引用次数: 0

Exercise reverses high-fat diet-induced perivascular adipose tissue dysfunction through modulation of UCP2 and TXNIP/NLRP3 pathways. 运动通过调节UCP2和TXNIP/NLRP3通路逆转高脂饮食诱导的血管周围脂肪组织功能障碍。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-02 DOI: 10.1007/s13105-026-01163-5

Jing Hu, Xi Jiang, Mingxing Ding, Sang Ki Lee, Lifeng Wang, Ting Li, Wei Li, Mallikarjuna Korivi

{"title":"Exercise reverses high-fat diet-induced perivascular adipose tissue dysfunction through modulation of UCP2 and TXNIP/NLRP3 pathways.","authors":"Jing Hu, Xi Jiang, Mingxing Ding, Sang Ki Lee, Lifeng Wang, Ting Li, Wei Li, Mallikarjuna Korivi","doi":"10.1007/s13105-026-01163-5","DOIUrl":"10.1007/s13105-026-01163-5","url":null,"abstract":"Perivascular adipose tissue (PVAT) dysfunction is associated with impaired vascular contractile properties, oxidative stress, and inflammation. We investigated the protective effect of exercise training against high-fat diet (HFD)-induced PVAT dysfunction, and explored the underlying molecular events in oxidative stress, endoplasmic reticulum (ER) stress and inflammation. Six-week-old male Sprague-Dawley rats were randomized into control, high-fat diet (HFD), and HFD plus exercise (HEx) groups. Following 6-week treatment, glycemic levels, vascular function, oxidative stress, ER stress, and inflammatory mediators were determined. We found that HFD-induced weight gain, hyperglycemia, and impaired vascular function were significantly attenuated by exercise training. HFD-induced redox imbalance in PVAT, represented by decreased antioxidant status and increased lipid peroxidation, was significantly inhibited by exercise. This was supported by a substantial restoration of UCP2 signaling and inhibition of p66shc, PKCβ, and Pin1 expressions in HEx group. Furthermore, exercise inhibited ER stress transducers, including IRE1, ATF6, eIF-2α, and GRP78, which were overexpressed with HFD. Inhibition of ER stress was accompanied by a significant inhibition of pro-inflammatory (NF-κB, TNF-α, IL-6, TXNIP, and NLRP3) and restoration of anti-inflammatory (FGF21) mediators against HFD. Exercise further reversed the transcriptional activation and deposition of NLRP3 inflammasome in PVAT. Exercise also reversed the HFD-induced macrophage polarization, as visualized by stabilized CD206 and iNOS levels. Exercise can restore HFD-induced vascular dysfunctions by promoting the UCP2 signaling and inhibiting the ER stress-associated TXNIP/NLRP3-mediated inflammatory response in PVAT.","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":"147326417","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}

引用次数: 0

Research progress of ferroptosis in obesity and its complications. 肥胖患者铁下垂及其并发症的研究进展。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-02 DOI: 10.1007/s13105-026-01156-4

Jiamei Zhang, Mengmeng Tang, Min Yu

引用次数: 0

Lipoxin A4 activates Nrf2 expression and mitigates hyperglycaemia-induced impairment of myogenesis and rescues damage to mitochondria. 脂素A4激活Nrf2表达，减轻高血糖诱导的肌生成损伤，并挽救线粒体损伤。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-03-02 DOI: 10.1007/s13105-026-01166-2

Akash Mitra, Deepika Bhat K, Joel Rimson Pinto, Samanwita Mandal, Undurti Narasimha Das, Bipasha Bose, Sudheer Shenoy P

{"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":"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.","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}

引用次数: 0