Journal of physiology and biochemistry最新文献

{"title":"Downhill running induced mitophagy in rat soleus muscle via the AMPK pathway.","authors":"Huayu Shang, Ranggui Ma, Shengju Chen, Hao Deng, Mengyu Li, Shiqiao Zheng, He Zhang, Duo Zhang, Tianai Yang, Ying Yang, Zhi Xia","doi":"10.1007/s13105-025-01093-8","DOIUrl":"https://doi.org/10.1007/s13105-025-01093-8","url":null,"abstract":"<p><p>Eccentric exercise is known to induce more pronounced muscle damage associated with delayed-onset muscle soreness than concentric exercise. This study aimed to investigate whether AMP-activated protein kinase (AMPK) pathway participates in control of mitophagy in rat skeletal muscle in response to downhill running. Eighty-eight male Sprague-Dawley rats were exercised on a treadmill tilted at 16° decline at 16 m·min^- 1 for 90 min, with the soleus muscle sampled at 0 h, 12 h, 24 h, 48 h and 72 h after exercise. The AMPK inhibitor compound C or AMPK activator AICAR or saline was injected intraperitoneally 20 min before exercise. After downhill treadmill running, the skeletal muscle mitochondrial structure appeared to be abnormal and contained mitophagosomes; the expression levels of AMPK phosphorylation, cyclophilin D (CypD), cytochrome C (CytC), mitochondrial FK506-binding protein 8 (FKBP8), microtubule-associated protein 1 light chain 3 (LC3), and the co-localization of FKBP8 with LC3 and mitochondria with dynamin-related protein 1 (Drp1), lysosomal-associated membrane protein 2 (LAMP2) were significantly higher; the expression levels of mechanistic target of rapamycin (mTOR Ser2448) phosphorylation and heat shock protein 60 (HSP60), mitochondrial respiratory complex I (NDUFB8) and complex III (UQCRC2), and adenosine triphosphate (ATP) content were significantly lower than those in the C group. Further study showed that the effect of downhill treadmill running was partly blocked by compound C and strengthened by AICAR. A session of downhill treadmill running activated the AMPK pathway and promoted LC3 co-localizations with mitochondria and FKBP8, and induced mitophagy and mitochondrial damage within rat skeletal muscle.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144136276","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":"Mechanisms underlying obesity-malignancy connection: a systematic narrative review.","authors":"Ayesha Sultana, Sobia Rana","doi":"10.1007/s13105-025-01084-9","DOIUrl":"https://doi.org/10.1007/s13105-025-01084-9","url":null,"abstract":"<p><p>The association between obesity and cancer risk carries substantial public health ramifications as obesity promotes cancer advancement via many cellular and molecular mechanisms. This study utilizes Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and narrative systematic review guidelines to evaluate 221 research articles selected from an initial collection of 1,288 publications sourced from multiple databases. Obesity-driven cancer risk is linked to hormonal imbalances including increased oestrogen levels that heighten the likelihood of breast and endometrial cancers, and insulin resistance that activates the insulin/ Insulin and Insulin-like Growth Factor 1 (IGF-1) pathway promoting colorectal cancer progression. Chronic low-grade inflammation, metabolic dysfunction, and hypoxia in expanding adipose tissue contribute to pancreatic, oesophageal, colorectal, renal, and liver malignancies. Recent research has identified novel mechanisms that drive obesity-induced cancer progression. The adipose tissue secretome, extracellular vesicle-mediated lipid and RNA transfer, ferroptosis resistance, and metabolic reprogramming via Cluster of Differentiation 36 (CD36), Fatty Acid Binding Protein 4 (FABP4), and Carnitine Palmitoyl transferase 1A (CPT1A) create a tumour-permissive microenvironment. Obesity-induced epigenetic memory sustains cancer risk even after weight loss through persistent histone modifications (Histone H3 Lysine 4 Trimethylation (H3K4me3), Histone H3 Lysine 27 Trimethylation (H3K27me3), DNA methylation, and RNA modifications, particularly through the Fat Mass and Obesity-Associated (FTO) gene. Additionally, organ and cell size expansion increase mutation susceptibility. Emerging pathways including the Von Hippel-Lindau (VHL)-Hypoxia-Inducible Factor (HIF) axis, PR Domain Zinc Finger Protein 16 (PRDM16)/Uncoupling Protein 1 (UCP1) inhibition, Signal Transducer and Activator of Transcription 3 (STAT3)-driven FABP4 upregulation, and Yes-Associated Protein (YAP)/Transcriptional Co-Activator with PDZ-Binding Motif (TAZ) signalling, further highlight obesity's role in oncogenesis. Future research should investigate weight-loss drugs' effects on cancer pathways, expand demographic diversity, and develop biomarkers for adiposity. Integrating Mendelian randomization, multi-omics, and artificial intelligence could reveal novel therapeutic targets. A comprehensive prevention strategy combining lifestyle interventions, pharmacological therapies, and biomarker-driven diagnostics is crucial to reducing obesity-related cancer burden and improving patient outcomes.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127921","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":"Molecular mechanisms of UCP1-independent thermogenesis: the role of futile cycles in energy dissipation.","authors":"Quanhao Sun, Xinyue Cui, Dong Yin, Juan Li, Jiarui Li, Likun Du","doi":"10.1007/s13105-025-01090-x","DOIUrl":"https://doi.org/10.1007/s13105-025-01090-x","url":null,"abstract":"<p><p>Adipose tissue thermogenesis has emerged as a prominent research focus for the treatment of metabolic diseases, particularly through mitochondrial uncoupling, which oxidizes nutrients to produce heat rather than synthesizing ATP. Uncoupling protein 1 (UCP1) has garnered significant attention as a core protein mediating non-shivering thermogenesis(NST). However, recent studies indicate that energy dissipation can also occur via UCP1-independent thermogenesis, partially driven by futile metabolic cycles. These cycles involve ATP depletion coupled with reversible energy reactions, resulting in futile energy expenditure. Unlike classical UCP1-mediated thermogenesis, futile cycling is not confined to brown and beige adipose tissue, suggesting a broader range of therapeutic targets. These findings open new avenues for targeting these pathways to enhance metabolic health. This review explores the characteristics and distinctions of the primary metabolic organs (adipose tissue, liver, and skeletal muscle) involved in the futile cycles of thermogenesis. It further elaborates on the cellular and molecular mechanisms underlying calcium, creatine, and lipid cycling, emphasizing their strengths, limitations, and roles beyond thermogenesis.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086388","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":"Acute pancreatitis experimental models, advantages and disadvantages.","authors":"Genaro J Rosales-Muñoz, Verónica Souza-Arroyo, Leticia Bucio-Ortiz, Roxana U Miranda-Labra, Luis E Gomez-Quiroz, María Concepción Gutiérrez-Ruiz","doi":"10.1007/s13105-025-01091-w","DOIUrl":"10.1007/s13105-025-01091-w","url":null,"abstract":"<p><p>Acute pancreatitis represents a severe health problem, not only because of the number of people affected but also because of the severity of its clinical presentation that can eventually lead to the death of patients. The study of the disease is complex, and we lack optimized models that can approach the clinical presentation in patients, in addition to the significant vulnerability of the organ itself. In the present work, we undertook the task of reviewing and analyzing the experimental methods most currently used for the induction of acute pancreatitis, emphasizing the advantages and disadvantages of each model and their delimitation based on experimental objectives. We aimed to provide an actual and quick-access guide for researchers interested in experimental acute pancreatitis.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086366","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":"Effects of high-intensity interval training on metabolic impairments in liver tissue of rats with type 2 diabetes: a metabolomics-based approach.","authors":"Kayvan Khoramipour, Mohammad Amin Rajizadeh, Mohammad Khaksari, Mansour Aminzadeh, Paula Crespo-Escobar, Alejandro Santos-Lozano, Mohammad Arjmand","doi":"10.1007/s13105-025-01085-8","DOIUrl":"https://doi.org/10.1007/s13105-025-01085-8","url":null,"abstract":"<p><p>Our aim was to study the metabolic effects of eight weeks of high-intensity interval training (HIIT) on the liver of rats with type 2 diabetes (T2D) using untargeted metabolomics. Twenty male Wistar rats, were divided into four groups (n = 5 per group): control (CTL), type 2 diabetes (DB), HIIT (EX), and type 2 diabetes + HIIT (DTX). A two months of a high-fat diet followed by a single dose of streptozotocin (35 mg/kg body weight) was used to induce T2D. Animals in the EX and DTX groups were trained for eight weeks (5 times per week, 4-10 running intervals at 80-100% of their maximum velocity). Metabolomic data were collected using proton nuclear magnetic resonance (¹H-NMR) to assess metabolic changes in the liver after training. Data were then pre-processed using ProMetab (MATLAB) for baseline correction, normalisation and binning. Fasting blood glucose (FBG) levels were analysed using a repeated-measures mixed ANOVA [i.e., time as the within-subject factor (Baseline - Month 0, Post-induction - Month 2, and Post-intervention - Month 4) and gruop (CTL, DB, HIIT, DTX) as the between-subject factor]. A one-way ANOVA with Tukey's post hoc test (p < 0.05) was applied to assess differences in Homeostatic Model Assessment for Insulin Resistance (HOMA-IR). Multivariate analysis - using sparse partial least squares discriminant analysis (sPLS-DA) - was performed to identify key metabolites, followed by pathway analysis (MetaboAnalyst) to determine significantly affected metabolic pathways. DB group showed higher HOMA-IR than CTL and DTX groups (p < 0.05). Furthermore, distinct clustering patterns was shown for metabolites by multivariate analysis. Key altered metabolic pathways included valine, leucine, and isoleucine biosynthesis; glutathione metabolism; pantothenate and coenzyme A biosynthesis; fructose and mannose metabolism; glycine, serine, and threonine metabolism; cysteine and methionine metabolism; arginine biosynthesis; tyrosine metabolism; histidine metabolism; beta-alanine metabolism; propanoate metabolism; glycolysis/gluconeogenesis; phenylalanine, tyrosine, and tryptophan biosynthesis; arginine and proline metabolism; and thiamine metabolism. These results suggest that eight weeks of HIIT may reverse metabolic changes induced by T2D in the rat liver, potentially contributing to reduced FBG and HOMA-IR levels. Clinical trial number: Not applicable.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078613","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":"Interplay between NETosis and the lncRNA-microRNA regulatory axis in the immunopathogenesis of cancer.","authors":"Nisreen Salah Majeed, Mohammed Hashim Mohammed, Zainab Amer Hatem, Amr Ali Mohamed Abdelgawwad El-Sehrawy, Subbulakshmi Ganesan, Abhayveer Singh, Marwa Azeez Akoul, Puneet Sudan, Roshni Singh, Hamad Ali Hamad","doi":"10.1007/s13105-025-01082-x","DOIUrl":"https://doi.org/10.1007/s13105-025-01082-x","url":null,"abstract":"<p><p>Neutrophil extracellular traps (NETs), web-like complex structures secreted by neutrophils, have emerged as key players in the modulation of immune responses and the immunopathogenesis of immune disorders. Initially described for their antimicrobial function, NETs now play a part in the fundamental processes of cancer biology, including cancer initiation, metastatic dissemination, and immune evasion strategies. NETs hijack anti-tumor immunity by entrapping circulating cancer cells, fostering the growth of tumors, and reorganizing the tumor microenvironment such that it is pro-malignancy. Emerging evidence emphasizes the role of NETosis coupled with non-coding RNAs-long non-coding RNAs (lncRNAs) and microRNAs (miRNAs)-as key regulators of gene expression and controllers of processes vital for cancer growth, such as immune response and programmed cell death processes like apoptosis, necroptosis, pyroptosis, and ferroptosis. Aberrantly expressed non-coding RNAs have been attributed to immune dysregulation and excessive NET production, promoting tumor growth. NETs are also associated with a myriad of pathological conditions, such as autoimmune disorders, cystic fibrosis, sepsis, and thrombotic disorders. New therapeutic approaches-such as DNase therapy and PAD4 inhibitors-target NET production and their degradation to modify immune function and the efficiency of immunotherapies. Further clarification of the intricate interactions of NETosis, lncRNAs, and miRNAs has the potential to establish new strategies for the suppression of the growth of tumors and preventing immune evasion. This review seeks to elucidate the interactions between NETosis and the regulatory networks involving non-coding RNAs that significantly contribute to the immunopathogenesis of cancer.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144016189","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":"Alterations in hepatic amino acid metabolism related to MASLD in individuals with obesity.","authors":"Armando J Pérez-Díaz, Inmaculada Ros-Madrid, María A Martínez-Sánchez, Sara Rico-Chazarra, Alba Oliva-Bolarín, Andrés Balaguer-Román, Virginia E Fernández-Ruiz, Carlos M Martínez, José E Yuste, Mercedes Ferrer-Gómez, Camilo J Llamoza-Torres, María D Frutos, María Á Núñez-Sánchez, Bruno Ramos-Molina","doi":"10.1007/s13105-025-01086-7","DOIUrl":"https://doi.org/10.1007/s13105-025-01086-7","url":null,"abstract":"<p><p>Deregulation of amino acid (AA) metabolism has been reported in several pathological conditions, including metabolic diseases (e.g., obesity and diabetes), cardiovascular diseases, and cancer. However, the role of alterations in AA levels in chronic liver disorders such as metabolic dysfunction-associated steatotic liver disease (MASLD) remains largely unexplored. In this study we aimed to evaluate the hepatic AA composition in patients with different stages of MASLD, and their relationship with MASLD-related risk factors. A case-control study was conducted in 40 patients with obesity undergoing bariatric surgery at Virgen de la Arrixaca University Hospital (Murcia, Spain), where MASLD diagnosis was confirmed by histological analysis of liver biopsies, and hepatic AA levels were measured using ultra-performance liquid chromatography high-resolution time-of-flight mass spectrometry. Our results revealed that the hepatic AA profile was significantly altered in patients with MASLD. More specifically, comparison between MASLD patients revealed a significant increase in hepatic levels of arginine, glycine and cystine in MASH samples compared to steatotic livers. In addition, hepatic concentrations of arginine, lysine and cystine positively correlated with histopathological diagnosis and other MASLD-related parameters, including transaminases and CK-18 levels. These findings suggest that alterations in certain hepatic AA levels such as arginine, lysine, glycine and cystine in MASLD patients could have translational relevance in understanding the onset of this disease.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144031013","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":"Oleoylethanolamine precursor triggers lipolysis during Time-Restricted Intermittent Fasting and promotes longevity and healthy aging of Caenorhabditis elegans.","authors":"Thondimuthu Vinitha, Rajasekharan Sharika, Krishnaswamy Balamurugan","doi":"10.1007/s13105-025-01087-6","DOIUrl":"https://doi.org/10.1007/s13105-025-01087-6","url":null,"abstract":"<p><p>Intermittent fasting (IF), Time-Restricted Intermittent Fasting (TRIF), and fasting-mimicking diets have gained popularity among weight loss programs. The body efficiently utilizes its energy reserves to activate metabolic processes in response to food intake. Modifying food regimens can alter/extend life span and promote healthy aging by activating specific metabolic processes. However, changes in general lipid metabolism, especially the alteration in N-acylethanolamide (NAE) regulation and their role in promoting lipolysis and extending life span during TRIF, are still inadequately explored. To bridge the knowledge gap, this study focuses on enhancing Oleoylethanolamine (OEA), a precursor molecule that instigates satiety, promotes lipolysis and extends the life span of model system, Caenorhabditis elegans. TRIF regimen in C. elegans induces OEA, which in turn lead to satiety followed by lipolysis and ATP synthesis. Lipolysis is stimulated by the increase in Adipose Tissue Triglyceride Lipase-1 (ATGL-1) activity that results from the enrichment in OEA precursor. In addition, the TRIF regimen induces oxidative stress resistance in C. elegans. Subsequently, this promotes longevity and slow aging in C. elegans by altering the insulin/ insulin-like growth factor signaling (IIS) pathway. The present study suggested the beneficial effects of time-restricted fasting in the eukaryotic model nematodes through the activation of lipid metabolism that involves enhanced production of OEA precursors which promotes lipolysis. In addition, the data revealed that the increased ATP production resulted in oxidative stress tolerance that promoted longevity and slow aging processes.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005948","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":"Activation of TRPA1 prevents metabolic dysfunction-associated steatotic liver disease in diet-induced obese mice through stimulating the AMPK/CPT1A signaling pathway.","authors":"Dan Wang, Sen Liu, Jindong Wan, Shichao Chen, Kaige Feng, Jixin Hou, Yi Yang, Peijian Wang","doi":"10.1007/s13105-025-01081-y","DOIUrl":"https://doi.org/10.1007/s13105-025-01081-y","url":null,"abstract":"<p><p>Mitochondrial dysfunction plays an important role in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). Transient receptor potential ankyrin-1 (TRPA1) activation improves mitochondrial dysfunction in a variety of cells. The present study tested the effects of Trpa1 knockout and activation in diet-induced MASLD in mice and palmitate-induced lipid deposition in HepG2 cells. Mice were fed with a high-fat diet (HFD) for 24 weeks to establish the animal model of MASLD. TRPA1 was downregulated in the liver of mice with MASLD and in HepG2 cells with palmitate-treated steatosis. Compared with HFD-fed wild-type mice, Trpa1^-/- mice on HFD demonstrated exacerbated lipid deposition and mitochondrial damage in hepatocytes. AMP-activated protein kinase (AMPK) and carnitine palmitoyl transferase 1 A (CPT1A) in the liver were downregulated by HFD and to a greater extent in Trpa1^-/- mice. Similarly, knockdown of Trpa1 worsened palmitate-induced lipid accumulation, mitochondrial morphological damage, mitochondrial ATP reduction and dysfunction, and downregulation of AMPK and CPT1A in HepG2 cells. Oral administration of cinnamaldehyde significantly reduced lipid deposition and improved mitochondrial damage in hepatocytes, which were abolished by HC030031, a TRPA1 antagonist. In HepG2 cells, cinnamaldehyde remarkably attenuated palmitate-induced lipid accumulation, mitochondrial damage, ATP reduction, and mitochondrial dysfunction, which were blunted by HC030031. Cinnamaldehyde reversed downregulation of AMPK and CPT1A in the liver of HFD-fed mice and palmitate-treated HepG2 cells through activating TRPA1. In conclusion, these findings suggest that the downregulation of TRPA1 may be involved in the pathogenesis of MASLD and activation of TRPA1 holds potential in the prevention and treatment of MASLD.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001109","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":"Ferroptosis in immune chaos: Unraveling its impact on disease and therapeutic potential.","authors":"Thanyaporn Direksunthorn, Abdulrahman T Ahmed, Nakaraj Pluetrattanabha, Subasini Uthirapathy, Suhas Ballal, Abhayveer Singh, Hussein Riyadh Abdul Kareem Al-Hetty, Anita Devi, Girish Chandra Sharma, Alexey Yumashev","doi":"10.1007/s13105-025-01078-7","DOIUrl":"https://doi.org/10.1007/s13105-025-01078-7","url":null,"abstract":"<p><p>Since its introduction in 2012, ferroptosis has garnered significant attention from researchers over the past decade. Unlike autophagy and apoptosis, ferroptosis is an atypical iron-dependent programmed cell death that falls under necrosis. It is regulated by various cellular metabolic and signaling processes, which encompass amino acid, lipid, iron, and mitochondrial metabolism. The initiation of ferroptosis occurs through iron-dependent phospholipid peroxidation. Notably, ferroptosis exhibits a dual effect and is associated with various diseases. A significant challenge lies in managing autoimmune disorders with unknown origins that stem from the reactivation of the immune system. Two contributing factors to autoimmunity are the aberrant stimulation of cell death and the inadequate clearance of dead cells, which can expose or release intracellular components that activate the immune response. Ferroptosis is distinct from other forms of cell death, such as apoptosis, necroptosis, autophagy, and pyroptosis, due to its unique morphological, biochemical, and genetic characteristics and specific relationship with cellular iron levels. Recent studies indicate that immune cells can both induce and undergo ferroptosis. To better understand how ferroptosis influences immune responses and its imbalance in disease, a molecular understanding of the relationship between ferroptosis and immunity is essential. Consequently, further research is needed to develop immunotherapeutics that target ferroptosis. This review primarily focuses on the role of ferroptosis in immune-related disorders.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998061","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}