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Annual review of physiology最新文献

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Beyond Digestion: Secretin as a Key Regulator of Systemic pH. 超越消化：分泌素作为系统pH值的关键调节器。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-10-16 DOI: 10.1146/annurev-physiol-040425-040843
Jesper Frank Andersen, Jens Leipziger, Peder Berg
{"title":"Beyond Digestion: Secretin as a Key Regulator of Systemic pH.","authors":"Jesper Frank Andersen, Jens Leipziger, Peder Berg","doi":"10.1146/annurev-physiol-040425-040843","DOIUrl":"https://doi.org/10.1146/annurev-physiol-040425-040843","url":null,"abstract":"<p><p>Secretin is a broad activator of epithelial bicarbonate secretion and regulates local and systemic pH balance along with metabolic functions. Its receptor, widely expressed across epithelial and neuroendocrine tissues, enables coordinated responses to digestive phases, systemic alkalosis, and volume regulation. This positions secretin as a corrective hormone of the postprandial alkaline tide and a critical signaling pathway in the prevention of excessive systemic alkalosis. Its signaling intersects with the renin-angiotensin-aldosterone system, where secretin, angiotensin II, and aldosterone jointly enhance pendrin-mediated chloride reabsorption and bicarbonate secretion during states such as Cl- depletion alkalosis. Conditions with disrupted secretin signaling, most notably cystic fibrosis, demonstrate the physiological importance of secretin-dependent bicarbonate secretion in pancreatic, biliary, renal, and potentially airway epithelia. Overall, secretin emerges not only as a gastrointestinal regulator but also as a central, integrative hormone linking digestion, metabolism, local and systemic acid-base homeostasis, renal electrolyte handling, and systemic volume regulation.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Manipulating the Rat Embryo: Genetic and Stem Cell-Based Technologies for Physiological Research. 操纵大鼠胚胎：生理研究的遗传和干细胞技术。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-10-16 DOI: 10.1146/annurev-physiol-040425-100916
Toshihiro Kobayashi, Masumi Hirabayashi
{"title":"Manipulating the Rat Embryo: Genetic and Stem Cell-Based Technologies for Physiological Research.","authors":"Toshihiro Kobayashi, Masumi Hirabayashi","doi":"10.1146/annurev-physiol-040425-100916","DOIUrl":"https://doi.org/10.1146/annurev-physiol-040425-100916","url":null,"abstract":"<p><p>Laboratory rats (<i>Rattus norvegicus</i>) have been invaluable to biomedical research and are well-suited for physiological analyses. Nevertheless, technical challenges in embryo and genetic manipulation have historically hindered the generation of genetically modified rats, thereby limiting their use for in vivo functional genetic studies. Recent advances, including genome editing and pluripotent/germline stem cell technologies, have substantially expanded rat genetic engineering. This review summarizes the historical background and recent advances in rat embryo manipulation and highlights the rapid development of genetic tools in rats, now catching up with those available in mice. These advances provide an opportunity to reassess the value of rats as experimental models. Furthermore, the combined use of mice and rats, exemplified by interspecific chimeras and comparative studies, offers new insights into conserved and species-specific physiological mechanisms across mammals.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 Brain-Gut-Microbiome Axis: Exploring the Link Between Depression and Irritable Bowel Syndrome. 脑-肠-微生物轴：探索抑郁症和肠易激综合征之间的联系。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-10-14 DOI: 10.1146/annurev-physiol-040225-111420
Lin Chang, Nelson B Freimer, Elaine Y Hsiao
{"title":"The Brain-Gut-Microbiome Axis: Exploring the Link Between Depression and Irritable Bowel Syndrome.","authors":"Lin Chang, Nelson B Freimer, Elaine Y Hsiao","doi":"10.1146/annurev-physiol-040225-111420","DOIUrl":"https://doi.org/10.1146/annurev-physiol-040225-111420","url":null,"abstract":"<p><p>The brain-gut-microbiome system is an integrated communication network linking the central nervous system, enteric nervous system, immune pathways, and intestinal microbiota. Increasing evidence indicates that dysregulation of this bidirectional signaling system contributes to both gastrointestinal and psychiatric disorders. Irritable bowel syndrome (IBS), a disorder of gut-brain interaction, and major depressive disorder (MDD) frequently coexist and share multiple biological and environmental risk factors. Advances in microbiome science, neuroimaging, and multi-omics technologies have revealed that microbial metabolites, neuroimmune signaling, and stress-responsive neuroendocrine pathways influence neural circuits regulating mood, visceral perception, and gastrointestinal function. These interconnected mechanisms may explain the high comorbidity between IBS and MDD and suggest that both conditions arise from disturbances across overlapping biological systems. In this review, we synthesize current knowledge of genetic, neurobiological, and potential microbial contributors to IBS and depression, discuss emerging therapeutic approaches targeting the brain-gut-microbiome system, and highlight future directions for developing mechanistically informed treatment strategies.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
An Agenda for Physiology in the Age of Artificial Intelligence. 人工智能时代的生理学议程。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-10-14 DOI: 10.1146/annurev-physiol-051926-033337
L Fernando Santana, David A Eisner, Yvonne Janssen-Heininger, Anne Joutel, Juanita L Merchant, Philipp E Scherer, Mohamed Trebak, Paul A Welling, Mark T Nelson, Kenneth Walsh
{"title":"An Agenda for Physiology in the Age of Artificial Intelligence.","authors":"L Fernando Santana, David A Eisner, Yvonne Janssen-Heininger, Anne Joutel, Juanita L Merchant, Philipp E Scherer, Mohamed Trebak, Paul A Welling, Mark T Nelson, Kenneth Walsh","doi":"10.1146/annurev-physiol-051926-033337","DOIUrl":"https://doi.org/10.1146/annurev-physiol-051926-033337","url":null,"abstract":"","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"1-0"},"PeriodicalIF":20.3,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Vascular Physiology and Pregnancy Complications. 血管生理学和妊娠并发症。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-09-24 DOI: 10.1146/annurev-physiol-040425-100711
Amanda A de Oliveira, Mariane Bertagnolli, Sandra T Davidge
{"title":"Vascular Physiology and Pregnancy Complications.","authors":"Amanda A de Oliveira, Mariane Bertagnolli, Sandra T Davidge","doi":"10.1146/annurev-physiol-040425-100711","DOIUrl":"https://doi.org/10.1146/annurev-physiol-040425-100711","url":null,"abstract":"<p><p>Maternal vascular adaptations to pregnancy optimize uterine and fetoplacental perfusion. When vascular remodeling and/or function are impaired, the maternal circulation may fail to meet the physiological demands of pregnancy, thereby increasing the risk of complications. The most common complications of pregnancy affecting maternal vascular health include hypertensive disorders of pregnancy, particularly preeclampsia; infectious or autoimmune diseases that often induce a preeclampsia-like phenotype; metabolic disorders such as gestational diabetes mellitus and excessive hypercholesterolemia; and advanced maternal age. Moreover, women with a history of a complicated pregnancy have an increased risk of developing later-life cardiovascular disease, representing a sex-specific risk factor. This review summarizes the mechanisms underlying vascular adaptations to pregnancy and examines how abnormal vascular changes within and beyond the uteroplacental circulation contribute to the development of pregnancy complications, as well as how these complications, in turn, affect maternal vascular health during pregnancy and later in life, focusing on underlying mechanisms.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Leptin: 30 Years Later. 瘦素：30年后。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-02-01 Epub Date: 2025-10-03 DOI: 10.1146/annurev-physiol-042324-100259
Rexford S Ahima, Jeffrey S Flier
{"title":"Leptin: 30 Years Later.","authors":"Rexford S Ahima, Jeffrey S Flier","doi":"10.1146/annurev-physiol-042324-100259","DOIUrl":"10.1146/annurev-physiol-042324-100259","url":null,"abstract":"<p><p>The discovery of leptin as an adipocyte-secreted hormone encoded by the <i>ob</i> gene whose absence produces severe obesity that is corrected by leptin repletion in both mice and humans was a transformative event in metabolic science. Leptin's discovery in 1994 accelerated the identification of central neuronal circuitry responsive to peripheral signals that regulate energy balance as well as metabolic, neuroendocrine, and other vital functions. Leptin's primary physiological role was initially viewed as preventing obesity by its levels rising, but subsequent research has emphasized the key role of falling levels to signal starvation. Resistance to leptin action, though partial, characterizes common forms of obesity. Despite much being learned about leptin signal transduction over 30 years, the precise molecular mechanisms for leptin resistance and common obesity remain unclear. Leptin therapy is effective in rare patients with congenital leptin deficiency and other low leptin conditions but not common obesity. Interestingly, reducing hyperleptinemia may prove useful in treating common obesity.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"229-250"},"PeriodicalIF":20.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145224853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Mechanisms and Therapies of Hypertrophic Cardiomyopathy. 肥厚性心肌病的机制和治疗。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-02-01 Epub Date: 2025-11-07 DOI: 10.1146/annurev-physiol-042224-093244
Niels Pietsch, Sonia R Singh, Lucie Carrier
{"title":"Mechanisms and Therapies of Hypertrophic Cardiomyopathy.","authors":"Niels Pietsch, Sonia R Singh, Lucie Carrier","doi":"10.1146/annurev-physiol-042224-093244","DOIUrl":"10.1146/annurev-physiol-042224-093244","url":null,"abstract":"<p><p>Hypertrophic cardiomyopathy (HCM) is the most common myocardial genetic disease characterized by left ventricular hypertrophy (LVH) and diastolic dysfunction with preserved or elevated ejection fraction. Thirty-five years after the identification of the first genetic variant in myosin heavy chain 7, other variants have been discovered in numerous components of the sarcomere, pointing to a primary defect in cardiomyocyte contractility. Still, a large portion of HCM patients does not have a pathogenic variant and others present with LVH of another genetic origin. Research has uncovered a primary driver of hypercontractility at the sarcomere level and diverse molecular and cellular mechanisms contributing to HCM, including alterations of calcium handling and proteolysis, microtubule modifications, energy deficiency, and the impact of noncardiomyocyte cell types. These discoveries have fueled preclinical and translational research, leading to the development of myosin inhibitors, which are now on the market, and gene-based therapeutic products. This review summarizes current knowledge on the genetics, mechanisms, and targeted treatments of HCM.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"155-181"},"PeriodicalIF":20.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145470568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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 Physiological Challenge of Climate Change for Free-Living Terrestrial Mammals. 气候变化对陆生哺乳动物的生理挑战。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-02-01 DOI: 10.1146/annurev-physiol-052824-091026
Andrea Fuller, Duncan Mitchell, Shane K Maloney
{"title":"The Physiological Challenge of Climate Change for Free-Living Terrestrial Mammals.","authors":"Andrea Fuller, Duncan Mitchell, Shane K Maloney","doi":"10.1146/annurev-physiol-052824-091026","DOIUrl":"10.1146/annurev-physiol-052824-091026","url":null,"abstract":"<p><p>Most scenarios that seek to predict the responses of terrestrial mammals to climate change focus on the direct thermal effects of higher ambient temperatures. Measurements from free-living mammals reveal that the physiological challenge for many terrestrial mammals facing climate change will arise from the compound effects of higher heat loads, reduced water, and reduced energy intake. Deaths from climate change, particularly for large mammals, are more likely to result from starvation than from heat stroke. The extent of heterothermy exhibited by a mammal, which results from the relaxation of temperature regulation in response to demands from competing homeostatic systems, provides an index of its physiological welfare and, therefore, a tool to assess sensitivity and responses to climate change. Studies of responses to heat in laboratory or captive individuals can identify what mammals can achieve physiologically, but they do not necessarily reveal what an animal will actually do in its natural habitat.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":"88 1","pages":"1-20"},"PeriodicalIF":20.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146155837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Mechanobiology and Resolution of Lung Fibrosis. 肺纤维化的力学生物学和解决方案。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-02-01 Epub Date: 2025-11-12 DOI: 10.1146/annurev-physiol-031725-021041
Patrick A Link, Daniel J Tschumperlin
{"title":"Mechanobiology and Resolution of Lung Fibrosis.","authors":"Patrick A Link, Daniel J Tschumperlin","doi":"10.1146/annurev-physiol-031725-021041","DOIUrl":"10.1146/annurev-physiol-031725-021041","url":null,"abstract":"<p><p>Pulmonary fibrosis is a devastating and progressive disease marked by replacement of gas-exchanging tissue with collagen-rich scar. The mechanical environment is profoundly altered in pulmonary fibrosis and contributes to disease progression via feedback relationships between cells, the extracellular matrix, and the evolving mechanical environment. Targeting these mechanobiological feedback loops has emerged as a promising approach to interrupt disease progression, though with challenges in how to intervene selectively, safely, and effectively. We posit that further delineation of cell-matrix mechanobiological interactions will be pivotal to promoting fibrosis resolution and should guide efforts to discover and implement new approaches that can preserve or even restore lung function. To set the stage for these advances, we first review the mechanobiology of the healthy lung and the feedback loops that promote fibrosis progression. We then lay out the challenges and opportunities for targeting the fibrotic matrix as an essential element for protecting or restoring lung function.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"487-511"},"PeriodicalIF":20.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13003399/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145501732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Decoding Connexin Hemichannels: Structure, Function, and Regulatory Mechanisms. 解码连接蛋白半通道：结构、功能和调节机制。
IF 20.3 1区 医学
Annual review of physiology Pub Date : 2026-02-01 Epub Date: 2025-11-11 DOI: 10.1146/annurev-physiol-050724-010008
Isaac E García, Jorge E Contreras
{"title":"Decoding Connexin Hemichannels: Structure, Function, and Regulatory Mechanisms.","authors":"Isaac E García, Jorge E Contreras","doi":"10.1146/annurev-physiol-050724-010008","DOIUrl":"10.1146/annurev-physiol-050724-010008","url":null,"abstract":"<p><p>Connexin hemichannels are pivotal for cellular communication, acting as independent conduits for ion and metabolite exchange, as well as precursors to gap junction channels. While their involvement in pathophysiological conditions, including cardiovascular, neurodegenerative, and inflammatory diseases, is well-documented, their physiological roles in tissue homeostasis and cellular signaling remain under active investigation. Despite considerable progress, our understanding of the mechanisms governing hemichannel gating, permeation, structural dynamics, and regulation remains incomplete. This review summarizes key foundational insights into recent advancements to offer a comprehensive perspective on hemichannel function. We explore the molecular determinants of hemichannel opening and closing, their interactions with cellular signaling networks, and structural adaptations that modulate permeation and gating. By integrating these findings, we highlight emerging concepts in connexin hemichannel regulation and underscore their potential as novel therapeutic targets in a variety of disease contexts.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"73-98"},"PeriodicalIF":20.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145493778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
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