Journal of physiology and biochemistry最新文献

{"title":"Renal proteomics of male offspring exposed to maternal protein restriction: molecular, epigenetic, and nephron-specific signatures of metabolic programming.","authors":"Danielle Amanda Niz Alvarez, Isabelle Tenori Ribeiro, Matheus Naia Fioretto, Marina Pereira Pires, Luisa Annibal Barata, Flávia Alessandra Maciel, Luiz Marcos Frediane Portela, Renato Mattos, Hecttor Sebastian Baptista, Pedro Menchini Vitali, Vinicius Alexandre Andrade Felipe, Marcel Rodrigues Ferreira, Elena Zambrano, Patrícia Aline Boer, Luis Antonio Justulin","doi":"10.1007/s13105-026-01189-9","DOIUrl":"10.1007/s13105-026-01189-9","url":null,"abstract":"<p><p>Chronic kidney disease is an increasing global public health concern, and the Developmental Origins of Health and Disease (DOHaD) concept proposes that adverse conditions during critical developmental windows predispose offspring to chronic disorders later in life. Maternal protein restriction (MPR), a well-established experimental model reflecting food insecurity, has been shown to impair nephrogenesis and promote long-term renal dysfunction. In this study, we investigated renal metabolic-epigenetic programming induced by gestational and lactational MPR in post-weaning male rats using a global kidney proteomic approach. MPR altered renal structure and profoundly dysregulated protein networks, characterized by downregulation of energy metabolism, ion transport, cytoskeletal organization, membrane integrity, and mitochondrial function, alongside upregulation of innate immune pathways, glutathione metabolism, vesicular trafficking, and cytoskeletal dynamics. Integrated pathway and disease enrichment analyses revealed the potential risk to hypertension, acid-base imbalance, renal tubular transport disorders, nephrosis, and renal failure. Key differentially expressed proteins (e.g., GPX1, CYCS, ATP1A2/ATP1B1, TUBB/TUBA isoforms, ANPEP, and metabolic enzymes) emerged as potential biomarkers of renal metabolic-epigenetic programming. Collectively, these findings identify molecular signatures that link early-life protein restriction to long-term risk of kidney disease and provide mechanistic insight into the nephron- and cell-specific consequences of MPR.</p>","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/PMC13149610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839155","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":"Hypoxia-inducible factor-1α: Dual roles in maintaining neuronal homeostasis and neuronal degeneration via regulation of oxidative stress, mitochondrial dynamics, and bioenergetics.","authors":"Saipriya Parol Puthusseri, Sruthy Ravivarma, Merin Johny, Ajith Vengellur","doi":"10.1007/s13105-026-01187-x","DOIUrl":"10.1007/s13105-026-01187-x","url":null,"abstract":"<p><p>Hypoxia-inducible factor-1α (HIF-1α) is an oxygen-sensitive transcription factor with an inherently paradoxical biology: under mild-to-moderate hypoxic stress, it functions as a pro-survival regulator, yet under severe or prolonged hypoxia, the same signalling axis promotes apoptotic and autophagic cell death. This duality carries particular significance in neurons, where HIF-1α serves as a critical nexus among neuronal survival, metabolic adaptation, and mitochondrial integrity, and where the consequences of its dysregulation are most profound given their exceptional metabolic demands and limited regenerative capacity. This review examines the molecular determinants governing this protective-to-detrimental switch, integrating key interconnected dimensions: the context-dependent regulation of oxidative stress, the control of mitochondrial bioenergetics, dynamics, mitophagy, and axonal transport; the dual role of HIF-1α in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and cerebral ischemia; and the therapeutic implications of precision-targeted HIF-1α modulation. Across all these contexts, a consistent pattern emerges: early or acute HIF-1α activation is broadly neuroprotective, while chronic or severe hypoxic stress converts the same pathway into a driver of neurodegeneration. Understanding the determinants of this switch, including hypoxia duration, severity, and cell-type specificity, provides a framework for designing temporally precise therapeutic interventions for hypoxia-related neurological disorders.</p>","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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839238","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 acute, subacute, and chronic exercise on plasma s-Klotho levels: a systematic review and meta-analysis.","authors":"Túlio Medina Dutra de Oliveira, Diogo Carvalho Felício, Taynara da Silva Ribeiro, José Elias Filho, Francisco José Amaro-Gahete, Giovani Bernardo Costa, Jorge Willian Leandro Nascimento, Maycon de Moura Reboredo, Carla Malaguti","doi":"10.1007/s13105-026-01182-2","DOIUrl":"10.1007/s13105-026-01182-2","url":null,"abstract":"<p><p>Exercise exerts beneficial effects on multiple physiological systems, influencing biomarkers associated with aging processes and chronic diseases. This systematic review and meta-analysis aimed to evaluate the acute, subacute, and chronic effects of exercise on s-Klotho levels in healthy individuals and patients with chronic diseases. A comprehensive search was conducted in electronic databases. Included studies were randomized and non-randomized studies assessing the effects of aerobic, resistance, or combined exercise on s-Klotho levels. Interventions were classified as acute (single session), subacute (< 12 weeks), or chronic (≥ 12 weeks). Risk of bias was assessed using RoB 2 and ROBINS-I tools, and quality of evidence was evaluated with the GRADE framework. Forty-one studies were included in the qualitative synthesis, and 30 in the meta-analysis, comprising 2,765 participants (18-85 years). Twenty-five involved healthy individuals, while 21 included patients with chronic diseases. Acute and subacute aerobic exercise increased s-Klotho levels in healthy individuals (SMD 0.69; 95%CI 0.41-0.97) and diseased populations (SMD 0.62; 95%CI 0.11-1.12). Chronic exercise (12-36 weeks) showed significant increases in healthy (SMD 0.57; 95%CI 0.33-0.82) and diseased populations (SMD 1.51; 95%CI 0.87-2.16). Resistance exercise thrice weekly demonstrated the highest effect (SMD 1.60; 95%CI 0.81-2.38). Most studies had high risk of bias, with quality of evidence ranging from very low to moderate. Exercise significantly increases s-Klotho levels, with acute and subacute aerobic sessions benefiting healthy and diseased populations, while chronic resistance exercise elicited greater responses in diseased populations. Despite promising findings, low methodological quality suggests cautious interpretation.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13134988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147815476","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":"Heme oxygenase-1 induction by hemin: a novel approach to enhance mitochondrial turnover and mitigate diet-induced liver damage.","authors":"Morena Wiszniewski, Lilian J Caldareri, Diego Mori, Federico Jara, Cora B Cymeryng, Esteban M Repetto","doi":"10.1007/s13105-026-01183-1","DOIUrl":"10.1007/s13105-026-01183-1","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by lipid accumulation and inflammatory injury. Kupffer cells (KC) play a key role in the immune response and metabolic homeostasis in the liver. We evaluated the impact of hemin treatment on the phenotype of KC and on metabolism and mitochondrial dynamics of hepatocytes in a rat model of early-stage MASH induced by a high-carbohydrate diet. In the liver, HO-1 induction by hemin was associated with reduced tissue injury and apoptosis, restored oxidative balance, attenuated UPR activation, reinstated autophagic flux and improved mitochondrial dynamics. In addition, hemin treatment enhanced fatty acid oxidation and insulin sensitivity in a KC-independent manner. These results suggest that hemin treatment exerts hepatoprotective effects in a rat model of early-stage MASH, highlighting the potential of this treatment as a therapeutic approach for MASH.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774688","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":"Research progress on PANoptosis in diabetic cardiomyopathy.","authors":"Chu Chen, Canran Lv, Peng Zhu, Zihao Chen, Jian Yang, Jing Zhang","doi":"10.1007/s13105-026-01180-4","DOIUrl":"10.1007/s13105-026-01180-4","url":null,"abstract":"<p><p>PANoptosis is a novel form of cell death that combines features of pyroptosis, apoptosis, and necroptosis. This process can be induced by various stimuli and involves the integration of multiple pro-cell death components, which assemble into different types of large molecular complexes known as PANoptosomes. Its regulatory mechanism involves several upstream key molecules, including Interferon Regulatory Factor 1, Transforming Growth Factor-β-Activated Kinase 1, and Adenosine Deaminase Acting on RNA 1, which collectively contribute to the initiation and execution of PANoptosis. Targeting the associated regulatory pathways represents an effective strategy for modulating PANoptosis. Given its significant role in cardiovascular diseases, modulating the activation of PANoptosis—either through promotion or inhibition—may offer a promising approach to preventing the progression of various related conditions. This review summarizes the current understanding of PANoptosis mechanisms and recent advances in research on its critical role in diabetic cardiomyopathy. It also highlights the complex crosstalk among multiple programmed cell death pathways, aiming to provide novel insights into effective therapeutic strategies for diabetic cardiomyopathy.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774677","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":"Machine learning-based prediction model for drug target identification and MASH improvement: a comprehensive analysis of biochemical and ferroptosis/autophagy biomarkers.","authors":"Marwa Matboli, Aly Elanwar, Radwa Khaled, Abdelrahman Khaled, Eman Hamdy Badr Eltantawy, Ghada Galal Hamam, Manar Yehia Ahmed, Manar Fouad, Ahmed Asmaa Tarek, Maryam Elmasry, Marwa M El-Shafei, Basma Emad Aboulhoda, Gouda Ibrahim Diab, Ibrahim H Aboughaleb","doi":"10.1007/s13105-026-01181-3","DOIUrl":"10.1007/s13105-026-01181-3","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD), marked by excess fat in the liver, has become the most prevalent chronic liver disease worldwide, affecting over 30% of adults. Its advanced form, metabolic dysfunction associated steatohepatitis (MASH), includes liver ballooning, and inflammation, and can progress to cirrhosis and hepatocellular carcinoma (HCC). Despite the increasing burden, effective pharmacotherapies for MASLD/MASH are still lacking. Programmed cell death mechanisms, such as autophagy and ferroptosis, are critical in the pathology of MASLD, influencing liver inflammation, fibrosis, and malignant transformation. This study employed six machine learning models—Random Forest, Logistic Regression, Extra Trees Classifier, Linear Discriminant Analysis, and Light Gradient Boosting Machine—to identify significant drug targets using Febuxostat, Perindopril, Amlodipine, and Atorvastatin, evaluated through molecular, biochemical, immunohistochemical, and pathological markers. We identified genes associated with MASH using microarray datasets from the Gene Expression Omnibus database, followed by protein-protein interaction and functional enrichment analyses to select genes related to ferroptosis, autophagy, and their epigenetic regulators (miRNAs-LncRNAs) in MASH-induced rats. Quantitative real-time PCR validated the expression of selected networks (mRNAs-miRNAs-LncRNAs). Additionally, we measured biochemical, inflammatory, and liver pathology markers to ensure the model’s robustness. Our results identified 16 out of 29 valuable therapeutic targets with an accuracy of 88.74% and an AUC of 0.9745, including LPCAT3, HGS, TSG101, SNF8, rno-miR-27a-5p, rno-miR-329-5p, CTBP1-AS2, ALT, AST, ALP, GGT, D. Bilirubin, Albumin, TMAO, GPX4, and TGFβ1.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13121215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774722","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":"Exploring the effects of lifelong aerobic exercise on early skeletal muscle remodeling between 8 and 14 months in the rat.","authors":"Alexandra Moreira-Pais, Rita Ferreira, Maria João Neuparth, Margarida Fardilha, Daniel Moreira-Gonçalves, Paula A Oliveira, José A Duarte","doi":"10.1007/s13105-026-01178-y","DOIUrl":"10.1007/s13105-026-01178-y","url":null,"abstract":"<p><p>The insidious onset and progression of sarcopenia make it vital to understand the early skeletal muscle changes and explore therapies to slow its progression. This study explored the gastrocnemius remodeling at an early stage of aging (14 months of age) and the effects of lifelong aerobic exercise. For that, 2-month-old male Wistar rats underwent a 12-month treadmill exercise program. Sedentary age-matched, young sedentary, and young exercised for 6 months rats were considered. The results highlighted an age-related decrease in the relative gastrocnemius muscle mass, suggestive of loss or atrophy of some fibers, which was mitigated by lifelong aerobic exercise. Consequently, an age-related compensatory hypertrophy was suggested to be triggered in the gastrocnemius muscle. Data proposed that aging reduced mitochondrial density, indicated by citrate synthase (CS) activity, which was prevented by lifelong aerobic exercise. The reduced CS activity correlated with increased ATP-dependent 6-phosphofructokinase (PFKM)/ATP synthase subunit beta (ATPB) ratio, suggesting that at an early stage of aging, the skeletal muscle favors the glycolytic metabolism in response to decreased mitochondrial content. The results also pointed to an age-induced AMP-activated protein kinase (AMPK) activation and an AMPK-related apoptosis inhibition, perchance to reduce fiber loss or atrophy. The basal phosphorylated AMPK/AMPK ratio decreased with lifelong aerobic exercise, possibly reflecting the exercise-induced increase in CS activity. This work highlights the importance of studying early skeletal muscle changes in aging for timely disease management and prevention.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13091809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717114","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":"Advances and challenges of ferroptosis in tumor immunity.","authors":"Yanfang Liu, Shiwan Lin, Zining Zhang, Dongqing Wang, Baiqing Fu","doi":"10.1007/s13105-026-01144-8","DOIUrl":"10.1007/s13105-026-01144-8","url":null,"abstract":"<p><p>Ferroptosis is a variant of regulated cell death elicited by iron dependent phospholipid peroxidation, represented for a robust therapy approach for the refractory tumor. In addition to kill cancer cells, ferroptosis could also elicited the immune response. The immunogenicity of ferroptosis resulted from both the immunogenicity of ferroptotic cell death and the effect of ferroptosis inducers on immune cells. The significantly varied susceptibility of immune cells to ferroptosis inducers may exert either enhance or inhibit cancer cells ferroptosis. Thus, the net immunomodulatory effect of ferroptosis may exhibit either immunostimulatory or immunoinhibitory. In this review, we firstly summarize immunogenicity of ferroptosis cancer cells. Then, we comprehensively and detailed discusses the versatile and complex ferroptosis immunomodulatory effective based crosstalk between cancer cells and various immune cells in the tumor microenvironment (TME), hoping to shed new light on novel strategies to promote immunotherapy efficacy by targeting ferroptosis.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717092","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":"Roles of extracellular vesicles in the pathogenesis of chronic myeloid leukemia.","authors":"Tereza Hrdinova, Helena Kupcova Skalnikova","doi":"10.1007/s13105-026-01184-0","DOIUrl":"10.1007/s13105-026-01184-0","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) are lipid bilayer-enclosed particles released by cells into the extracellular space. They are produced by the majority of cell types under both physiological and pathological conditions. EVs mediate intercellular communication by delivering bioactive molecules - such as RNAs, adhesion molecules, signaling mediators, and antigen-presenting molecules - to recipient cells, thereby modulating their phenotype and function. A growing body of evidence highlights the involvement of EVs in the pathophysiology of leukemia, including their roles in remodeling the bone marrow microenvironment, promoting angiogenesis, enabling immune evasion, regulating apoptosis, and contributing to drug resistance. Beyond their functional roles, EVs are emerging as promising diagnostic and prognostic biomarkers, as well as potential drug delivery vehicles. This review first outlines key aspects of chronic myeloid leukemia and the bone marrow niche, and then focuses on the current understanding of how EVs contribute to the transformation of a normal bone marrow environment into a leukemic one. Finally, we discuss the potential applications of EVs as biomarkers and therapeutic delivery systems in chronic myeloid leukemia.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13090219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717055","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":"Profibrotic macrophage populations and cell communications in pulmonary fibrosis.","authors":"Dengfeng Zhang, Wenyue Zhao, Chang Xu, Liqing Du, Qiang Liu","doi":"10.1007/s13105-026-01179-x","DOIUrl":"10.1007/s13105-026-01179-x","url":null,"abstract":"<p><p>Pulmonary fibrosis is a chronic inflammatory disorder marked by fibroblast activation, collagen deposition, thickening of the alveolar septum, and impaired lung function. Profibrotic macrophages play a pivotal role in driving inflammatory responses during the progression of pulmonary fibrosis and have emerged as promising therapeutic targets. Although distinct from classical M1/M2 macrophage phenotypes, profibrotic macrophages across various forms of pulmonary fibrosis exhibit shared transcriptomic profiles associated with fibrogenesis. This review aims to summarize the characteristics, origins, developmental trajectories, distribution, energy metabolism, and epigenetic regulation of profibrotic macrophage populations in different pulmonary fibrosis diseases and animal models. In the context of pulmonary fibrosis, these macrophages engage in robust crosstalk with non-immune cells in the lung—such as fibroblasts and type II alveolar epithelial cells—thereby exacerbating fibrotic processes. Consequently, strategies aimed at depleting profibrotic macrophages or disrupting their detrimental interactions with non-immune cells may show promise as potential therapeutic approaches to slow disease progression, offering new avenues for treatment.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147717098","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}