Comprehensive Physiology最新文献

Influence of Serum Vitamin D on Age-Related Physiological Changes: A Cross-Sectional Study in Middle-Aged Adults. 血清维生素D对年龄相关生理变化的影响：一项中年人横断面研究

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-10-01 DOI: 10.1002/cph4.70047

Poulami Dhar, Prajna Bhandary, Shailaja Moodithaya

{"title":"Influence of Serum Vitamin D on Age-Related Physiological Changes: A Cross-Sectional Study in Middle-Aged Adults.","authors":"Poulami Dhar, Prajna Bhandary, Shailaja Moodithaya","doi":"10.1002/cph4.70047","DOIUrl":"10.1002/cph4.70047","url":null,"abstract":"Background: The pace of physiological deterioration is variable among living beings. Vitamin D is proven to be one of the crucial yet deficient vitamins. Hypovitaminosis D is often marked by aging, but young adults are also not exempt. Thus, to identify the lacunae and bridge the gap between aging and vitamin D, this study selected the middle-aged age group and their phenotypic aging markers. Physiological changes are gradual and measurable using non-invasive methods, and they contribute to the phenotypic aging markers like BMI, WHR, F%, WS, and HGS. This study hypothesizes that the minute changes in phenotypic markers in young adults, which are prominent during middle age and potentially cause early aging, are influenced by Vitamin D.Methods: The study is based on a cross-sectional design. Healthy individuals were recruited from the OPD following convenience sampling, and anthropometric and physical assessments were performed. Then, the blood samples were assessed for vitamin D levels. After segregating deficient (< 20 ng/dL), insufficient (20-30 ng/mL), and sufficient (> 20 ng/dL), the comparison was drawn.Result: A frequency analysis of three groups and comparisons among them was made. Association of phenotypic markers with vitamin D was shown.Conclusion: The present study population attempted to establish the hypothesis; however, chronological age can have multicollinearity with all variables, and sample size is a limitation of this study.","PeriodicalId":10573,"journal":{"name":"Comprehensive Physiology","volume":"15 5","pages":"e70047"},"PeriodicalIF":5.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to "Influence of Serum Vitamin D on Age-Related Physiological Changes: A Cross-Sectional Study in Middle-Aged Adults". 修正了“血清维生素D对年龄相关生理变化的影响：一项中年人的横断面研究”。

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-10-01 DOI: 10.1002/cph4.70054

引用次数: 0

Understanding Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Physical Fatigue Through the Perspective of Immunosenescence. 从免疫衰老的角度理解肌痛性脑脊髓炎/慢性疲劳综合征体力疲劳。

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-10-01 DOI: 10.1002/cph4.70056

Yingzhe Luo, Huimin Xu, Shaoquan Xiong, Jianlong Ke

{"title":"Understanding Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Physical Fatigue Through the Perspective of Immunosenescence.","authors":"Yingzhe Luo, Huimin Xu, Shaoquan Xiong, Jianlong Ke","doi":"10.1002/cph4.70056","DOIUrl":"https://doi.org/10.1002/cph4.70056","url":null,"abstract":"Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating illness marked by persistent fatigue, yet its mechanisms remain unclear. Growing evidence implicates immunosenescence-the age-related decline in immune function-in the onset and persistence of fatigue.Methods: This review synthesizes clinical and experimental data to examine how immunosenescence contributes to ME/CFS. We focus on chronic inflammation, senescent immune phenotypes, mitochondrial dysfunction, and neuroendocrine imbalance, with emphasis on maladaptive crosstalk among immune, muscular, neuroendocrine, and vascular systems.Results: Aging immune cells drive chronic inflammation that impairs mitochondrial ATP production and promotes muscle catabolism. Concurrently, HPA-axis suppression and β2-adrenergic dysfunction amplify immune dysregulation and energy imbalance. Together, these processes illustrate how immunosenescence sustains pathological cross-organ signaling underlying systemic fatigue.Conclusion: Immunosenescence provides a unifying framework linking immune, metabolic, and neuroendocrine dysfunction in ME/CFS. Recognizing cross-organ communication highlights its clinical relevance, suggesting biomarkers such as cytokines and exhaustion markers, and supports integrated therapeutic strategies targeting immune and metabolic networks.","PeriodicalId":10573,"journal":{"name":"Comprehensive Physiology","volume":"15 5","pages":"e70056"},"PeriodicalIF":5.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Physiological Mechanisms Vulnerable to Alcohol-Induced Alterations: Role in Chronic Comorbidities. 易受酒精诱导改变的生理机制：在慢性合并症中的作用。

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-10-01 DOI: 10.1002/cph4.70057

Liz Simon, Kaitlin E Couvillion, Meagan E Donovan, Eden M Gallegos, Flavia M Souza-Smith, Patricia E Molina

{"title":"Physiological Mechanisms Vulnerable to Alcohol-Induced Alterations: Role in Chronic Comorbidities.","authors":"Liz Simon, Kaitlin E Couvillion, Meagan E Donovan, Eden M Gallegos, Flavia M Souza-Smith, Patricia E Molina","doi":"10.1002/cph4.70057","DOIUrl":"https://doi.org/10.1002/cph4.70057","url":null,"abstract":"Alcohol misuse is a leading modifiable risk factor for disease burden across the lifespan. Alcohol-mediated end organ injury results from a combination of pathophysiological processes including oxidative stress, mitochondrial dysfunction, cell death, endoplasmic reticulum stress, extracellular matrix remodeling, and epigenomic adaptations. Alcohol's multi-systemic physiological impact causes direct cellular damage and impairs an individual's capacity to adapt or recover from additional health insults, thereby amplifying overall disease burden. While the impact of alcohol on liver and brain physiological mechanisms is the most studied, the adverse effects of alcohol extend to multiple other organ systems, and though frequently underappreciated, contribute to several comorbidities. This review focuses on alcohol-associated pathophysiological effects on the gastrointestinal, cardiovascular, immune systems, and energy metabolism that contribute to multiorgan injury and disease burden. Understanding the pathophysiological effects of alcohol on the different organ systems will significantly help inform therapeutic modalities to help reduce alcohol-associated comorbidities.","PeriodicalId":10573,"journal":{"name":"Comprehensive Physiology","volume":"15 5","pages":"e70057"},"PeriodicalIF":5.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Holistic Researcher: A Day in the Life of Professor Faadiel Essop, Centre for Cardio-Metabolic Research in Africa (CARMA). 《整体研究者：非洲心脏代谢研究中心（CARMA） Faadiel Essop教授的一天》。

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-08-01 DOI: 10.1002/cph4.70036

Paul Trevorrow, Faadiel Essop

引用次数: 0

The Role of p53-Mediated Cellular Senescence in Idiopathic Pulmonary Fibrosis. p53介导的细胞衰老在特发性肺纤维化中的作用。

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-08-01 DOI: 10.1002/cph4.70041

Yueyuan Jin, Mengna Jiang, Wenxia Bu, Yifan Zhou, Juan Tang, Shan Bao, Rui Zhao, Xinyuan Zhao, Demin Cheng

{"title":"The Role of p53-Mediated Cellular Senescence in Idiopathic Pulmonary Fibrosis.","authors":"Yueyuan Jin, Mengna Jiang, Wenxia Bu, Yifan Zhou, Juan Tang, Shan Bao, Rui Zhao, Xinyuan Zhao, Demin Cheng","doi":"10.1002/cph4.70041","DOIUrl":"10.1002/cph4.70041","url":null,"abstract":"An increasing body of evidence suggests that cellular senescence is a risk factor for the development of idiopathic pulmonary fibrosis (IPF). Cellular senescence is a permanent state by which cells cease to divide and adopt an irreversible cell cycle arrest, which is believed to contribute to aging and aging-related diseases. IPF is an age-related, chronic, progressive, and ultimately fatal interstitial lung disease of unknown etiology. IPF is characterized by repeated alveolar epithelial cell damage, fibroblast proliferation, excessive extracellular matrix (ECM) deposition, impaired gas exchange, and death. As an important transcription factor, p53 is critically involved in the regulation of senescence and fibrosis-related diseases. The mechanism of p53-mediated cellular senescence in IPF remains poorly understood, particularly regarding therapeutic strategies targeting p53. In this review, we summarize p53's structure, function, and signaling in senescence-driven IPF, and explore p53-targeted interventions for IPF. In conclusion, p53 may be a potential therapeutic target for senescence and IPF.","PeriodicalId":10573,"journal":{"name":"Comprehensive Physiology","volume":"15 4","pages":"e70041"},"PeriodicalIF":5.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endothelial Glycocalyx: The Missing Link Between Angiogenic Imbalance in Preeclampsia and Systemic Inflammation in HELLP Syndrome. 内皮糖盏：子痫前期血管生成失衡与HELLP综合征全身性炎症之间的缺失环节。

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-08-01 DOI: 10.1002/cph4.70032

Anthony Atallah, Marie-Nathalie Sarda, Catherine McCarey, Jérôme Massardier, Cyril Huissoud

{"title":"Endothelial Glycocalyx: The Missing Link Between Angiogenic Imbalance in Preeclampsia and Systemic Inflammation in HELLP Syndrome.","authors":"Anthony Atallah, Marie-Nathalie Sarda, Catherine McCarey, Jérôme Massardier, Cyril Huissoud","doi":"10.1002/cph4.70032","DOIUrl":"10.1002/cph4.70032","url":null,"abstract":"The pathophysiology of preeclampsia and HELLP syndrome relies on systemic vascular endothelial dysfunction, resulting from angiogenic imbalance due to abnormal uteroplacental vascular remodeling and placental ischemia/reperfusion. Recent studies demonstrated that HELLP syndrome falls within the spectrum of secondary microangiopathy due to abnormal complement activation. However, to date, the link between angiogenic imbalance, endothelial dysfunction, and complement activation remains unclear. Building upon current understanding of complement regulation, this paper proposes a novel pathophysiological approach, suggesting a new understanding of HELLP syndrome and preeclampsia, including the undebatable role of sFlt-1/PlGF and the knowledge of maternal systemic endothelial and renal diseases. We hypothesize that endothelial glycocalyx may be the missing link between angiogenic factors, inflammatory regulation, and endothelial maternal lesions. Targeting the glycocalyx-endothelium axis may enable novel therapeutic strategies that delay delivery and reduce maternal-neonatal morbidity in preeclampsia and HELLP syndrome.","PeriodicalId":10573,"journal":{"name":"Comprehensive Physiology","volume":"15 4","pages":"e70032"},"PeriodicalIF":5.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12314582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HIF-Mediated Fructose Metabolism and Disease Progression in the Cardiovascular-Kidney-Metabolic Syndrome. hif介导的果糖代谢和心血管-肾-代谢综合征的疾病进展。

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-08-01 DOI: 10.1002/cph4.70033

David Mathew, Sean Davidson, Derek Yellon

{"title":"HIF-Mediated Fructose Metabolism and Disease Progression in the Cardiovascular-Kidney-Metabolic Syndrome.","authors":"David Mathew, Sean Davidson, Derek Yellon","doi":"10.1002/cph4.70033","DOIUrl":"10.1002/cph4.70033","url":null,"abstract":"The 'Cardiovascular-Kidney-Metabolic Syndrome' which is characterized by multi-organ dysfunction ultimately resulting in adverse cardiac outcomes, serves to highlight the importance of organ crosstalk in pathophysiology. The cellular metabolism of fructose, regulated by Ketohexokinase-C with associated inflammatory sequelae, is mechanistically linked with each component of this clinical entity. Fructose metabolism is confined to the Kidney, Liver, and Small Intestine under normal physiological conditions; however, in the context of ischaemia, HIF-1α induces cardiac expression of Ketohexokinase-C with consequent organ hypertrophy and dysfunction. This adverse effect of cardiac HIF-1α accumulation raises concerns over the potential pleiotropic effects of the 'HIF stabilizing' inhibitors of Prolyl Hydroxylase currently entering clinical practice for the treatment of anemia in Chronic Kidney Disease, particularly given the increased cardiovascular mortality observed in this patient group. We suggest that pleiotropic effects of 'HIF stabilization' on cardiac physiology warrant investigation and, furthermore, that pharmacological inhibition of Ketohexokinase-C, and therefore fructose metabolism, represents an opportunity to improve cardiac outcomes in the Cardiovascular-Kidney-Metabolic Syndrome.","PeriodicalId":10573,"journal":{"name":"Comprehensive Physiology","volume":"15 4","pages":"e70033"},"PeriodicalIF":5.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Crosstalk Between Microbiome and Ferroptosis in Diseases: From Mechanism to Therapy. 微生物群与疾病中铁下垂的串扰：从机制到治疗。

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-08-01 DOI: 10.1002/cph4.70042

Si-Qi Ding, Yun Lei, Zhe-Ming Zhao, Xin-Yun Li, Ji-Xuan Lang, Jia-Kui Zhang, Yong-Shuang Li, Chun-Dong Zhang, Dong-Qiu Dai

{"title":"Crosstalk Between Microbiome and Ferroptosis in Diseases: From Mechanism to Therapy.","authors":"Si-Qi Ding, Yun Lei, Zhe-Ming Zhao, Xin-Yun Li, Ji-Xuan Lang, Jia-Kui Zhang, Yong-Shuang Li, Chun-Dong Zhang, Dong-Qiu Dai","doi":"10.1002/cph4.70042","DOIUrl":"https://doi.org/10.1002/cph4.70042","url":null,"abstract":"The human microbiome is a unique organ and maintains host immunomodulation and nutrient metabolism. Structural and functional microbiome alterations are commonly known as dysbiosis, which is strongly associated with disease progression. Ferroptosis is a novel iron-dependent cell death mode characterized by intracellular iron accumulation, increased reactive oxygen species (ROS), and lipid peroxidation (LPO). Importantly, the complex crosstalk between the microbiome and ferroptosis in disease has attracted considerable research attention. The microbiome influences ferroptosis by regulating host iron homeostasis, mitochondrial metabolism, and LPO, among many other pathways. Thus, the in-depth analysis of microbiome-ferroptosis crosstalk and associated mechanisms could provide new strategies to treat human diseases. Therefore, understanding this crosstalk is critical. Here, we systematically explore the associations between gut microbiome and ferroptosis across multiple diseases. We show that the oral microbiome also influences disease progression by regulating ferroptosis. Furthermore, we provide a potential for certain disease therapies by targeting the crosstalk between the microbiome and ferroptosis.","PeriodicalId":10573,"journal":{"name":"Comprehensive Physiology","volume":"15 4","pages":"e70042"},"PeriodicalIF":5.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bile Acid Profile Differs Between Brain Regions in Rodents and Is Disrupted in a Rodent Model of Alzheimer's Disease. 啮齿动物脑区胆汁酸谱不同，在阿尔茨海默病啮齿动物模型中被破坏。

IF 5.2 2区医学

Comprehensive Physiology Pub Date : 2025-08-01 DOI: 10.1002/cph4.70034

Melanie A Reuter, Rosalinda Moreno, Madelynn E Agabao-Tucker, Rahaf Shishani, Jessica Miranda Bustamante, Zara Marfori, Taylor Richieri, Anthony E Valenzuela, Ameer Y Taha, Pamela J Lein, Renu Nandakumar, Bethany P Cummings

{"title":"Bile Acid Profile Differs Between Brain Regions in Rodents and Is Disrupted in a Rodent Model of Alzheimer's Disease.","authors":"Melanie A Reuter, Rosalinda Moreno, Madelynn E Agabao-Tucker, Rahaf Shishani, Jessica Miranda Bustamante, Zara Marfori, Taylor Richieri, Anthony E Valenzuela, Ameer Y Taha, Pamela J Lein, Renu Nandakumar, Bethany P Cummings","doi":"10.1002/cph4.70034","DOIUrl":"10.1002/cph4.70034","url":null,"abstract":"Low but biologically relevant levels of bile acids are found in the brain and are altered in patients with Alzheimer's disease (AD). However, the regulation of brain bile acid levels and what drives brain bile acid dynamics are poorly understood. Bile acids are synthesized in the liver and further metabolized by bacteria in the gut. Therefore, bile acids are mediators of the liver-brain axis and the gut-brain axis. Additionally, whether the bile acid profile differs between brain regions and whether the brain region-specific bile acid profile is impacted by disease, such as AD, is unknown. Therefore, we tested the hypothesis that the brain bile acid profile is influenced by peripheral bile acid metabolism, differs between brain regions, and that these dynamics change in AD. To this end, we assessed the bile acid profile in the cortex and hippocampus of wild-type mice maintained on different diets. To test the effect of AD, we used the TgF344-AD rat model. We found that the brain bile acid profile in mice was mildly altered by diet and, in both mice and rats, differs substantially between brain regions. For example, cholic acid and taurocholic acid are enriched in the cortex relative to the hippocampus in both mice and rats. Further, using a rat model of AD, we found that brain region differences in bile acid profiles are attenuated in AD. Together, these data demonstrate that both peripheral and central regulatory mechanisms maintain bile acid homeostasis in specific brain regions and that these homeostatic mechanisms are disrupted in AD.","PeriodicalId":10573,"journal":{"name":"Comprehensive Physiology","volume":"15 4","pages":"e70034"},"PeriodicalIF":5.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0