Journal of physiology and biochemistry最新文献_第6页

DGAT1 regulates keratinocyte proliferation through the modulation of retinoid homeostasis. DGAT1通过调节类视黄醇稳态调节角化细胞增殖。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-06-10 DOI: 10.1007/s13105-026-01196-w

Kamila Kwiecień, Natalia Bryniarska-Kubiak, Agnieszka Morytko, Alicja Uchańska, Maciej Pastuszczak, Marcin Migaczewski, Joanna Cichy, Patrycja Kwiecińska

{"title":"DGAT1 regulates keratinocyte proliferation through the modulation of retinoid homeostasis.","authors":"Kamila Kwiecień, Natalia Bryniarska-Kubiak, Agnieszka Morytko, Alicja Uchańska, Maciej Pastuszczak, Marcin Migaczewski, Joanna Cichy, Patrycja Kwiecińska","doi":"10.1007/s13105-026-01196-w","DOIUrl":"10.1007/s13105-026-01196-w","url":null,"abstract":"Multiple mechanisms contribute to skin barrier integrity, and emerging evidence suggests that acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1) plays a key role in its regulation through both lipid and retinoid metabolism. Although DGAT1 deficiency leads to cutaneous abnormalities, the direct role of DGAT1 in keratinocyte biology remains unclear. Here, we show that DGAT1 deficiency drives extensive keratinocyte hyperproliferation and barrier dysfunction under homeostatic conditions. Transcriptomic profiling revealed upregulation of genes associated with proliferation, inflammation, and retinoic acid (RA) signaling, consistent with increased proliferation observed in vitro and in vivo. Unexpectedly, while DGAT1 expression was elevated in human psoriatic lesions and in a murine psoriasis model, DGAT1 loss reduced keratinocyte proliferation in this inflammatory condition. Further analyses identified dysregulated RA signaling as a central mediator of these effects. DGAT1-deficient keratinocytes exhibited elevated RA-target gene expression and increased expression of RA-binding proteins, indicating enhanced RA bioavailability. Our findings establish DGAT1 as a context-dependent regulator of keratinocyte proliferation, promoting growth in homeostasis while restraining it in psoriasis. By linking DGAT1 activity with RA signaling, this work uncovers a previously unrecognized pathway contributing to epidermal physiology and inflammatory skin disease.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13253717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148218238","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}

引用次数: 0

TRIM38 alleviates the pathogenesis of diabetic nephropathy by suppressing NF-κB activation via inducing RIPK1 degradation. TRIM38通过诱导RIPK1降解抑制NF-κB活化，减轻糖尿病肾病的发病机制。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-06-03 DOI: 10.1007/s13105-026-01195-x

Yifan Fang, Xiaojuan Rao, Jianlin Dou, Pengyuan Zheng

{"title":"TRIM38 alleviates the pathogenesis of diabetic nephropathy by suppressing NF-κB activation via inducing RIPK1 degradation.","authors":"Yifan Fang, Xiaojuan Rao, Jianlin Dou, Pengyuan Zheng","doi":"10.1007/s13105-026-01195-x","DOIUrl":"10.1007/s13105-026-01195-x","url":null,"abstract":"Diabetic nephropathy (DN), a major microvascular complication of diabetes, remains a leading cause of end-stage renal disease. Tripartite motif protein 38 (TRIM38), a member of the TRIM family, plays critical roles in apoptosis, innate immunity, and inflammatory processes. Data of GEO database shows that TRIM38 is notably increased in the renal tubules of patients with DN. However, its functional significance in DN pathogenesis remains unexplored. In this study, streptozotocin (STZ)-induced diabetic mice and high glucose (HG)-treated HK-2 cells were employed to mimic DN conditions. Our results demonstrated that TRIM38 expression was significantly upregulated in renal tissues of DN patients, STZ-induced diabetic mice, and HG-stimulated HK-2 cells. Functionally, TRIM38 overexpression ameliorated renal dysfunction in diabetic mice and preserved the NAD+/NADH balance, while attenuating oxidative stress and inflammatory responses. Mechanistically, TRIM38 overexpression suppressed the NF-κB signaling activation. Further analysis revealed that TRIM38 physically interacted with receptor-interacting protein kinase 1 (RIPK1) and promoted its ubiquitination and degradation, thereby inhibiting the NF-κB pathway activation. Rescue experiments confirmed that RIPK1 overexpression abolished the protective effects of TRIM38 overexpression on HG-treated HK-2 cells. Our study identifies TRIM38 as a novel modulator of DN progression that exerts its protective effects by targeting RIPK1 degradation and subsequent inhibition of NF-κB signaling. These findings provide new insights into the molecular mechanisms underlying DN and highlight TRIM38 as a potential therapeutic target for DN treatment.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150197","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

Dietary bioactive compounds modulating satiety and appetite: mechanisms of action. 调节饱腹感和食欲的膳食生物活性化合物：作用机制。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-06-01 DOI: 10.1007/s13105-026-01185-z

Gema Casado-Hidalgo, Marián Pueyo-Arias, Katherine Gil-Cardoso, Francisco Les, Roger Mariné-Casadó, Montserrat Pinent, Anna Ardévol, Silvia Lorente-Cebrián, Frédéric Capel, Xavier Escoté, Fermin I Milagro, Víctor López

{"title":"Dietary bioactive compounds modulating satiety and appetite: mechanisms of action.","authors":"Gema Casado-Hidalgo, Marián Pueyo-Arias, Katherine Gil-Cardoso, Francisco Les, Roger Mariné-Casadó, Montserrat Pinent, Anna Ardévol, Silvia Lorente-Cebrián, Frédéric Capel, Xavier Escoté, Fermin I Milagro, Víctor López","doi":"10.1007/s13105-026-01185-z","DOIUrl":"10.1007/s13105-026-01185-z","url":null,"abstract":"Obesity and overweight represent critical public health problems worldwide, driving the search for effective strategies for their prevention and treatment. Modulating appetite and satiety through natural compounds present in the diet emerges as a promising approach to controlling energy intake and improving metabolic balance. This article reviews the molecular and physiological mechanisms involved in appetite regulation, including the function of gastrointestinal hormones (GLP-1, CCK, PYY, ghrelin), the role of the hypothalamus, and the influence of microbial metabolites such as short-chain fatty acids (SCFAs). Different groups of compounds such as fibres, proteins, lipids, polyphenols, saponins, and alkaloids are analyzed in relation to their capacity to modulate both orexigenic (ghrelin) and anorexigenic signals (GLP-1, CCK, PYY), as well as their broader effects on neuroendocrine and metabolic pathways. Despite the growing body of preclinical evidence, results in humans are still limited and, at times, inconsistent, underscoring the need for long-term controlled studies to clarify their mechanisms and clinical potential. This review provides a comprehensive overview of the pathways through which dietary bioactive compounds can contribute to appetite regulation, providing a scientific basis for the development of nutritional interventions aimed at combating obesity and related metabolic disorders.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148138246","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

Therapeutic effects of chitooligosaccharide-epigallocatechin gallate conjugate on NAFLD: impact on gut-liver axis, lipid metabolism, and inflammation in rats fed a high-fat diet. 壳寡糖-表没食子儿茶素没食子酸酯偶联物对NAFLD的治疗作用：对高脂饮食大鼠肠-肝轴、脂质代谢和炎症的影响

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-05-30 DOI: 10.1007/s13105-026-01193-z

Sirikul Mueangaun, Kanokrada Tonphu, Natcha Lerkdumnernkit, Jirakhamon Sengking, Jiraporn Tocharus, Soottawat Benjakul, Chainarong Tocharus

{"title":"Therapeutic effects of chitooligosaccharide-epigallocatechin gallate conjugate on NAFLD: impact on gut-liver axis, lipid metabolism, and inflammation in rats fed a high-fat diet.","authors":"Sirikul Mueangaun, Kanokrada Tonphu, Natcha Lerkdumnernkit, Jirakhamon Sengking, Jiraporn Tocharus, Soottawat Benjakul, Chainarong Tocharus","doi":"10.1007/s13105-026-01193-z","DOIUrl":"10.1007/s13105-026-01193-z","url":null,"abstract":"Non-alcoholic fatty liver disease (NAFLD) is a progressive disorder correlated with hepatic lipid homeostasis, gut dysbiosis, and inflammation. In this study, we propose a novel dietary therapy for NAFLD utilizing a conjugate of chitooligosaccharide (COS) and epigallocatechin gallate (EGCG), as the underlying mechanisms of NAFLD remain unclear. NAFLD was induced in male Wistar rats by administering a high-fat diet (HFD) for 16 weeks, followed by administration of COS-EGCG conjugate (150, 300, and 600 mg/kg) for an additional four weeks. The treatment alleviated metabolic parameters, liver steatosis, and injury. It also reduced hepatic lipid accumulation by downregulating the expression of CD36, fatty acid synthase (FASN), and sterol regulatory element-binding protein 1c (SREBP-1c), while upregulating peroxisome proliferator-activated receptor alpha (PPARα), carnitine palmitoyltransferase 1 A (CPT1A), and microsomal triglyceride transfer protein (MTTP). Regarding the gut-liver axis, the conjugate modulated gut microbiota, reduced serum lipopolysaccharide (LPS) levels, and restored the expression of intestinal tight junction proteins (zonula occludens-1; ZO-1 and occludin). It also prevented liver inflammation induced by gut-derived LPS by suppressing the Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway. The results suggest that the COS-EGCG conjugate exerts therapeutic effects against NAFLD by regulating hepatic lipid metabolism, modulating the gut microbiota, and attenuating gut-derived LPS-induced liver inflammation.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148101633","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

Evaluation of an experimental model of senescence SAMR1/SAMP8 for microRNA studies in acute myocardial infarction: role of sex and aging. 衰老实验模型SAMR1/SAMP8在急性心肌梗死中的microRNA研究：性别和衰老的作用

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-05-23 DOI: 10.1007/s13105-026-01194-y

A B Paes, B Descals-Beltrán, C Rosales-Ariza, A Díaz, D Pérez-Cremades, A P Dantas, C Hermenegildo, S Novella

{"title":"Evaluation of an experimental model of senescence SAMR1/SAMP8 for microRNA studies in acute myocardial infarction: role of sex and aging.","authors":"A B Paes, B Descals-Beltrán, C Rosales-Ariza, A Díaz, D Pérez-Cremades, A P Dantas, C Hermenegildo, S Novella","doi":"10.1007/s13105-026-01194-y","DOIUrl":"10.1007/s13105-026-01194-y","url":null,"abstract":"Age and sex are critical yet often overlooked variables in preclinical models of acute myocardial infarction (AMI), potentially limiting the translational relevance of molecular findings. In this study, we used the Senescence-Accelerated Mouse Prone 8 (SAMP8) strain, a model of age-related cardiovascular dysfunction, alongside age-matched SAMR1 controls, to investigate early expression patterns of four canonical circulating miRNA biomarkers of AMI: miR-1-3p, miR-133a-3p, miR-208a-3p, and miR-499-5p. Male and female mice underwent left anterior descending (LAD) coronary artery ligation, with serum and cardiac tissue collected at 1, 4, and 24 h post-injury. Results reveal a robust early induction of all four miRNAs in serum, with 4 h identified as the optimal profiling time point. Notably, miR-1-3p was significantly elevated in both male and female SAMP8 mice post-AMI, but not in SAMR1. miR-133a-3p increased only in aged females, while male SAMP8 and SAMR1 mice showed divergent responses. miR-208a-3p and miR-499-5p rose consistently across all groups. In cardiac tissue, SAMR1 mice exhibited downregulation of all four miRNAs, whereas only miR-1-3p was reduced in SAMP8 males. Baseline expression in sham-operated hearts revealed age-related differences, particularly in males, with lower levels of miR-133a-3p, miR-208a-3p, and miR-499-5p in SAMP8 versus SAMR1. These findings highlight pronounced age- and sex-dependent miRNA expression dynamics in both serum and cardiac tissue during the acute phase of AMI. These results validate the SAMP8/SAMR1 model as a valuable tool for dissecting molecular responses to myocardial injury and underscore the need to integrate age and sex into preclinical AMI research.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13198506/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148005639","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}

引用次数: 0

The progress of mitochondrial function and transfer in stem cell regulation and therapy. 线粒体功能与转移在干细胞调控与治疗中的研究进展。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-05-21 DOI: 10.1007/s13105-026-01192-0

Yubing Zhang, Zhuojian Qu, Zhiliang Guo, Lijuan Zhang, Hong Li, Xiaoyun Zhang, Xiumei Guan, Xiaodong Cui, Wenxu Wang, Min Cheng

{"title":"The progress of mitochondrial function and transfer in stem cell regulation and therapy.","authors":"Yubing Zhang, Zhuojian Qu, Zhiliang Guo, Lijuan Zhang, Hong Li, Xiaoyun Zhang, Xiumei Guan, Xiaodong Cui, Wenxu Wang, Min Cheng","doi":"10.1007/s13105-026-01192-0","DOIUrl":"10.1007/s13105-026-01192-0","url":null,"abstract":"Mitochondria, serving as central organelles for energy metabolism, play a critical regulatory role in stem cell self-renewal and differentiation-a function increasingly supported by accumulating evidence and closely linked to various aging-related diseases. Central to their function in stem cell pluripotency are several key mechanisms, such as the control of reactive oxygen species, mitophagy, and mitochondrial-endoplasmic reticulum communication. Mitochondrial transfer, as an emerging intercellular communication mechanism, can enhance stem cell pluripotency and function by replacing damaged mitochondria or activating mitophagy in recipient cells. However, different transfer mechanisms can induce distinct effects on recipient cells. The development of artificial mitochondrial transfer technology, compared to traditional cell transplantation, reduces immune rejection and offers new strategies for stem cell therapy. This review examines the interplay between mitochondrial function and stem cell fate determination, discusses the therapeutic potential of mitochondrial transfer in stem cell-based regenerative strategies, and establishes a theoretical framework for understanding and treating mitochondrial dysfunctions and aging-associated pathologies.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147982336","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

Abstracts of the XXXV Congress of the Spanish Nutrition Society/Sociedad Española de Nutrición (SEÑ) and XI Meeting of Young Researchers. 西班牙营养学会第三十五届大会/Sociedad Española de Nutrición （SEÑ）和第十一届青年研究人员会议摘要。

IF 4.3 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-05-19 DOI: 10.1007/s13105-026-01186-y

引用次数: 0

Chrono overexpression blunts exercise-induced improvement in muscular glucose metabolism by inhibiting the BMAL1 transcriptional activity in high-fat diet-fed mice. 在高脂饮食喂养的小鼠中，时间过表达通过抑制BMAL1转录活性，使运动诱导的肌肉葡萄糖代谢改善变得迟钝。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-05-14 DOI: 10.1007/s13105-026-01191-1

Lei Xu, Jie Jia, Lu Yan, Yangwenjie Wang, Shudan Miao, Ying Zhang

{"title":"Chrono overexpression blunts exercise-induced improvement in muscular glucose metabolism by inhibiting the BMAL1 transcriptional activity in high-fat diet-fed mice.","authors":"Lei Xu, Jie Jia, Lu Yan, Yangwenjie Wang, Shudan Miao, Ying Zhang","doi":"10.1007/s13105-026-01191-1","DOIUrl":"10.1007/s13105-026-01191-1","url":null,"abstract":"Aerobic exercise improves systemic insulin sensitivity by modulating muscle glucose metabolism. The CHRONO/BMAL1 pathway constitutes a core component of the endogenous molecular clock and participates in glucose metabolic regulation; however, whether it mediates exercise-induced metabolic benefits under high-fat diet (HFD) conditions remains unclear. We therefore investigated the role of this pathway in conferring protective effects of aerobic exercise against HFD-induced glucose metabolic dysfunction in skeletal muscle, by subjecting wild-type (WT) and inducible muscle-specific Chrono overexpression (Chrono IMOE) mice to an HFD with or without 12-week exercise. Unlike in WT mice, exercise failed to ameliorate adipose mass, dyslipidemia, and insulin resistance in HFD-fed Chrono IMOE mice. Mechanistically, in skeletal muscle of Chrono IMOE mice, Chrono overexpression suppressed exercise-induced reductions in CHRONO expression and CHRONO-BMAL1 binding, as well as the increase in BMAL1 levels. Consequently, despite elevated p-TBC1D1Ser237 and GLUT4 expression, exercise failed to promote GLUT4 sarcolemmal colocalization or upregulate gene expression of key enzymes for glycolysis and glycogen metabolism in skeletal muscle of Chrono IMOE mice. These findings demonstrate that preventing CHRONO‑BMAL1 dissociation via muscle-specific Chrono overexpression abrogates exercise-induced GLUT4 membrane trafficking, transcriptional activation of glycolytic/glycogen metabolic genes, and systemic insulin sensitivity improvements in HFD-fed mice, establishing CHRONO‑BMAL1 dissociation as a required step for these exercise adaptations.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147941761","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-induced modulation of the unfolded protein response: a therapeutic avenue for muscle wasting disorders. 运动诱导的未折叠蛋白反应的调节：肌肉萎缩障碍的治疗途径。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-05-11 DOI: 10.1007/s13105-026-01190-2

Ao Ke, Zhuo Jinyuan, Lijuan Xiang, Zhanguo Su

{"title":"Exercise-induced modulation of the unfolded protein response: a therapeutic avenue for muscle wasting disorders.","authors":"Ao Ke, Zhuo Jinyuan, Lijuan Xiang, Zhanguo Su","doi":"10.1007/s13105-026-01190-2","DOIUrl":"10.1007/s13105-026-01190-2","url":null,"abstract":"Muscle wasting, prevalent in various pathological conditions including cancer, cardiac dysfunction, and neurodegeneration, is typified by sustained protein depletion in muscle and a compromised ability of the tissue to repair and regenerate effectively. Triggered by disruptions in protein folding in the endoplasmic reticulum (ER), the unfolded protein response (UPR) represents a key regulatory system that sustains intracellular proteostasis under conditions of stress. While the UPR is crucial for cellular survival, prolonged activation or dysfunction of the pathway can contribute to muscle atrophy and the progression of muscle wasting diseases. Recent evidence suggests that exercise, through its impact on cellular stress responses, can modulate the UPR in muscle cells, promoting a protective response that enhances protein folding capacity, reduces ER stress, and stimulates muscle regeneration. This review explores how exercise influences the UPR in muscle cells, focusing on the activation of key UPR sensors, including IRE1, PERK, and ATF6, and their downstream effects on protein quality control, autophagy, and muscle fiber maintenance. We also examine the role of exercise in promoting adaptive responses in muscle cells, including increased mitochondrial function, autophagy, and the activation of stress resistance pathways, all of which can counteract muscle wasting. The review also emphasizes exercise as an effective strategy to influence ER stress pathways and attenuate muscle atrophy associated with pathological conditions, offering critical insights into the molecular benefits of physical activity for muscle preservation.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868836","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

Gut dysbiosis and nitric oxide dysregulation in cirrhosis progression: mechanistic insights and pathophysiological implications. 肝硬化进展中的肠道生态失调和一氧化氮失调：机制见解和病理生理意义。

IF 5.1 3区生物学

Journal of physiology and biochemistry Pub Date : 2026-05-07 DOI: 10.1007/s13105-026-01188-w

Vlad Răzniceanu, Andra Țichindeleanu, Eugen-Valentin Răducu, Șerban Ellias Trella, Iuliana Nenu

{"title":"Gut dysbiosis and nitric oxide dysregulation in cirrhosis progression: mechanistic insights and pathophysiological implications.","authors":"Vlad Răzniceanu, Andra Țichindeleanu, Eugen-Valentin Răducu, Șerban Ellias Trella, Iuliana Nenu","doi":"10.1007/s13105-026-01188-w","DOIUrl":"10.1007/s13105-026-01188-w","url":null,"abstract":"Cirrhosis represents the end stage of chronic liver injury, characterized by progressive fibrosis and architectural distortion that precipitate portal hypertension and systemic complications. Recent evidence positions gut microbiota dysbiosis and nitric oxide (NO) dysregulation as central, interacting pathophysiological mechanisms in cirrhosis progression. Intestinal barrier dysfunction facilitates bacterial translocation and thereby exposes the liver to lipopolysaccharides and pathogen-associated molecular patterns that trigger hepatic inflammation via Toll-like receptor signalling, a phenomenon aggravated by dysbiosis. This immune activation stimulates inducible NO synthase in Kupffer cells and systemic endothelium, generating excess NO that drives splanchnic vasodilation and worsens portal hypertension. Paradoxically, intrahepatic endothelial NO synthase activity becomes impaired, reducing sinusoidal NO availability and increasing intrahepatic vascular resistance. These interconnected disturbances perpetuate inflammation and fibrogenesis, contributing to cirrhosis decompensation and spontaneous bacterial peritonitis. Despite substantial mechanistic insight into these pathways, therapeutic translation remains limited. Statins show promise by restoring intrahepatic eNOS function and reducing portal pressure, while microbiota-targeted interventions (antibiotics, probiotics, fecal transplantation) address gut-derived inflammation. This review synthesizes our current understanding of the gut-liver-NO axis in cirrhosis, highlighting how dysbiosis and aberrant NO signalling reinforce each other through inflammatory feedback loops, and identifies critical gaps between mechanistic knowledge and clinical application that warrant further investigation.","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839231","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}

引用次数: 0