Nuraliah F Mohd Fadzli, Siti SM Al Bakri, Norshariza Nordin
{"title":"Corrigendum to “Centella asiatica as a potential neurotherapeutic adjunct in oxidative stress–targeted stem cell therapies” [Curr Opin Physiol, 46(2025) 1–7/100865]","authors":"Nuraliah F Mohd Fadzli, Siti SM Al Bakri, Norshariza Nordin","doi":"10.1016/j.cophys.2025.100873","DOIUrl":"10.1016/j.cophys.2025.100873","url":null,"abstract":"","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"46 ","pages":"Article 100873"},"PeriodicalIF":1.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145578607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shaira Gail Santos , Khaja Shameem Mohammed Abdul , Nicole H Purcell
{"title":"Protein phosphatases in metabolic dysfunction-associated steatotic liver disease: emerging mechanisms and therapeutic strategies","authors":"Shaira Gail Santos , Khaja Shameem Mohammed Abdul , Nicole H Purcell","doi":"10.1016/j.cophys.2025.100860","DOIUrl":"10.1016/j.cophys.2025.100860","url":null,"abstract":"<div><div>Metabolic dysfunction–associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease globally, with its severe form, metabolic dysfunction–associated steatohepatitis (MASH), increasing the risk of fibrosis, cirrhosis, and hepatocellular carcinoma. Despite its prevalence, there are limited FDA-approved therapies for MASLD, underscoring the need for novel treatment strategies. Protein phosphatases play critical roles in MASLD pathogenesis as key regulators of metabolic and inflammatory pathways. This review highlights specific phosphatases that are crucial in insulin signaling, lipid metabolism, inflammation, and fibrosis within the liver. While some phosphatases exacerbate disease progression by promoting liver dysfunction, others exhibit protective effects, suggesting potential as therapeutic targets. Altering phosphatase activity may reduce steatosis, improve insulin sensitivity, and alleviate fibrosis. Continued research is essential for developing selective modulators with minimal off-target effects, with the goal of identifying therapeutic approaches to prevent or reverse MASLD progression.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"46 ","pages":"Article 100860"},"PeriodicalIF":1.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145268665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Khaja Shameem Mohammed Abdul , Inca Stienhans , Shaira Gail Santos , Hollis Rausch , Nicole H Purcell
{"title":"Recent advances in PHLPP1 and PHLPP2 research: an update in the heart","authors":"Khaja Shameem Mohammed Abdul , Inca Stienhans , Shaira Gail Santos , Hollis Rausch , Nicole H Purcell","doi":"10.1016/j.cophys.2025.100867","DOIUrl":"10.1016/j.cophys.2025.100867","url":null,"abstract":"<div><div>In recent years, pleckstrin homology domain leucine-rich repeat protein phosphatase-1 (PHLPP1) and 2 (PHLPP2) have emerged as key players in regulating various survival signaling pathways, including Akt, and contribute towards cardiovascular disease development. This review highlights the diverse mechanisms regulating PHLPP1/2 at transcriptional, translational, and post-translational levels and discusses their role in cardiovascular function and disease. We further explore the therapeutic potential of targeting PHLPP1/2 using small molecule inhibitors, peptide inhibitors, microRNAs, long noncoding RNAs, and natural compounds. While the divergent roles of PHLPP1 and PHLPP2 in maintaining cellular homeostasis and their dysregulation in cancer and other diseases are well documented, their regulation and downstream targets in the heart under normal and pathological states remain unclear. Future studies are warranted to discover the regulatory mechanisms of PHLPP1/2, identify novel cardiac stress-regulated substrate kinases and binding partners, and develop therapies that target these phosphatases independently for clinical translation.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"46 ","pages":"Article 100867"},"PeriodicalIF":1.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145363063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yimin Li , Yuenuo Luo , Xiaodan Zhao , Shiying Wu , Ping Li
{"title":"Probiotics and antioxidants: synergistic mechanisms in reducing oxidative stress and anti-aging applications","authors":"Yimin Li , Yuenuo Luo , Xiaodan Zhao , Shiying Wu , Ping Li","doi":"10.1016/j.cophys.2025.100866","DOIUrl":"10.1016/j.cophys.2025.100866","url":null,"abstract":"<div><div>Oxidative stress is one of the important mechanisms leading to oxidative aging. The balance between intracellular oxidants and antioxidants is disrupted, resulting in DNA hydroxylation, protein denaturation, lipid peroxidation, and cell apoptosis, ultimately affecting the survival ability of cells. Probiotics and antioxidants are the main means of combating oxidative stress. In recent years, the limitations of using probiotics or antioxidants alone have become increasingly apparent, and the synergistic effect of probiotics and antioxidants has become a new research hotspot. This review synthesizes the current evidence on the synergistic roles of probiotics and antioxidants in mitigating oxidative stress and delaying aging, with an emphasis on mechanistic insights and translational potential.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"46 ","pages":"Article 100866"},"PeriodicalIF":1.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145417054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The link between circadian disruption and Alzheimer’s disease and related dementias: insights from peripheral inflammation","authors":"Carmalena V Cordi , Jennifer M Hurley","doi":"10.1016/j.cophys.2025.100859","DOIUrl":"10.1016/j.cophys.2025.100859","url":null,"abstract":"<div><div>Circadian rhythms are essential for maintaining physiological homeostasis, influencing biological processes from the sleep–wake cycle to metabolism and immune responses. Disruption of these rhythms is increasingly linked to the pathogenesis of Alzheimer’s disease and related dementias (ADRDs), conditions characterized by cognitive decline and neuropsychiatric symptoms through various pathways, including increases in inflammation. While many studies link the effects of circadian disruption on neuroinflammation to ADRDs, this review explores the potential link between the circadian disruption of peripheral inflammation and ADRDs. We discuss the evidence of how circadian misalignment can exacerbate neuroinflammation through the activation of the peripheral immune system. We further examine the role of peripheral factors such as insulin dysregulation, melatonin levels, and gut microbiome imbalances in amplifying these peripheral inflammatory responses. These data underscore the significance of circadian regulation in maintaining immune homeostasis, highlighting potential therapeutic avenues for mitigating ADRDs through the restoration of circadian integrity.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"46 ","pages":"Article 100859"},"PeriodicalIF":1.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145222481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Setor K Kunutsor , Khushmanjot Kaur , Ashish H Shah
{"title":"Sex differences in acute coronary syndrome outcomes and prognosis: a decade of progress and persistent disparities (2014–2025)","authors":"Setor K Kunutsor , Khushmanjot Kaur , Ashish H Shah","doi":"10.1016/j.cophys.2025.100868","DOIUrl":"10.1016/j.cophys.2025.100868","url":null,"abstract":"<div><div>Acute coronary syndrome (ACS) remains a global health challenge, with sex differences in outcomes persisting despite major advances in cardiovascular care. Women continue to experience worse short- and long-term outcomes than men, including higher mortality, complications, and hospital readmissions - particularly among younger women. These disparities reflect biological, psychosocial, and healthcare system factors, including delayed diagnosis and lower access to guideline-based interventions. Evidence from low- and middle-income countries, though limited, suggests similar or greater disparities. Most available data are from observational studies, with randomized trials rarely designed to assess sex-specific effects. Addressing these gaps requires sex-informed research, equitable care delivery, and risk prediction tools tailored by sex to improve ACS outcomes globally.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"46 ","pages":"Article 100868"},"PeriodicalIF":1.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145417053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jovana Joksimovic Jovic , Nikola Jovic , Maja Muric , Vladimir Jakovljevic
{"title":"Polycystic ovary syndrome and cardiometabolic risk: a perspective on women's heart health","authors":"Jovana Joksimovic Jovic , Nikola Jovic , Maja Muric , Vladimir Jakovljevic","doi":"10.1016/j.cophys.2025.100869","DOIUrl":"10.1016/j.cophys.2025.100869","url":null,"abstract":"<div><div>Polycystic ovary syndrome (PCOS) is the most prevalent endocrine disorder among women of reproductive age and is increasingly recognized as a cardiometabolic condition. In addition to reproductive abnormalities, PCOS is closely linked to an elevated risk of hypertension, insulin resistance, dyslipidemia, visceral adiposity, and early markers of atherosclerosis. Growing evidence indicates that androgen excess, endothelial dysfunction, and related molecular pathways contribute to adverse cardiovascular remodeling. This review integrates recent clinical and experimental findings connecting PCOS to cardiovascular disease (CVD), with particular emphasis on phenotypic variation, hormonal regulation, and sex-specific mechanisms. A better understanding of these interrelationships is essential to refine risk stratification and guide the development of targeted strategies aimed at preventing CVD in this high-risk female population.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"46 ","pages":"Article 100869"},"PeriodicalIF":1.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145417055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Visceral adipose tissue and the female heart: mechanisms and implications","authors":"Muhammad A Fahim , Yao Yao , Wanling Xuan","doi":"10.1016/j.cophys.2025.100871","DOIUrl":"10.1016/j.cophys.2025.100871","url":null,"abstract":"<div><div>Heart failure with preserved ejection fraction (HFpEF) is an increasingly prevalent clinical challenge, particularly among aging and postmenopausal women. Emerging evidence highlights a significant role of adipose tissue, especially adipose tissue surrounding the heart, in the pathogenesis of HFpEF. Visceral fat depots function as endocrine and inflammatory organs. Coupled with hormonal changes during menopause, adipose tissue contributes to cellular senescence and myocardial dysfunction. This brief review summarizes the mechanistic links among adipose tissue, sex hormones, and depot-specific inflammation in HFpEF, and underscores potential targets for future research and therapeutic intervention.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"46 ","pages":"Article 100871"},"PeriodicalIF":1.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145466714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sofia Tanveer, Akarsh Bajpai, Shweta Jitendra Rajput, Preethi Saravanan, Basant K Patel
{"title":"Targeting oxidative stress to combat neurodegenerative diseases, amyotrophic lateral sclerosis and Huntington’s, for better brain health and recovery","authors":"Sofia Tanveer, Akarsh Bajpai, Shweta Jitendra Rajput, Preethi Saravanan, Basant K Patel","doi":"10.1016/j.cophys.2025.100872","DOIUrl":"10.1016/j.cophys.2025.100872","url":null,"abstract":"<div><div>Amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD) are among neurodegenerative disorders (NDs) that are progressive, irreversible, debilitating and eventually lethal. Misfolding, aggregation and deposition of proteins such as mutant superoxide dismutase type-1 (SOD1), transactive response DNA-binding protein 43 (TDP-43) and fused in sarcoma (FUS) in ALS, and mutant huntingtin with polyglutamine expansion in HD, are implicated. Elevated level of reactive oxygen species, causing oxidative stress, is a pathological commonality among several NDs, including ALS and HD, which drives the damage to neuronal cell physiology and homeostasis. In view of its high potential as a therapeutic target, here, we review the role of oxidative stress in the pathogenesis of ALS and HD and the currently pursued therapies targeting oxidative stress, including the FDA-approved drugs and other novel therapeutic strategies presently under investigation.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"46 ","pages":"Article 100872"},"PeriodicalIF":1.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145528697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"From clock genes to exercise: shaping the field of Exercise Chronophysiology","authors":"Andrea Ciorciari , Katja A Lamia","doi":"10.1016/j.cophys.2025.100835","DOIUrl":"10.1016/j.cophys.2025.100835","url":null,"abstract":"<div><div>Circadian rhythms, regulated by central and peripheral clocks, shape physiological processes through clock gene activity and external cues, modulating metabolic pathways, hormonal regulation, and body temperature. By acting on these factors, exercise serves as a powerful zeitgeber, impacting the timing of biological functions. This review highlights insights from molecular to behavioral aspects, examining exercise's role in addressing circadian disruptions, its therapeutic potential for metabolic, psychiatric, and cancer-related conditions, and its applications in enhancing physical performance. Exercise Chronophysiology emerges as a promising integrative approach, offering innovative strategies for promoting health, preventing disease, and optimizing athletic performance.</div></div>","PeriodicalId":52156,"journal":{"name":"Current Opinion in Physiology","volume":"45 ","pages":"Article 100835"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144269988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}