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Annual review of physiology最新文献

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Leptin: 30 Years Later. 瘦素：30年后。
IF 19.1 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":19.1,"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 19.1 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":19.1,"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 19.1 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":"https://doi.org/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":19.1,"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
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 19.1 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":19.1,"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
Mechanobiology and Resolution of Lung Fibrosis. 肺纤维化的力学生物学和解决方案。
IF 19.1 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":19.1,"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
Calcium Regulation of Mitochondrial Metabolism. 钙对线粒体代谢的调节
IF 19.1 1区 医学
Annual review of physiology Pub Date : 2026-02-01 Epub Date: 2025-11-10 DOI: 10.1146/annurev-physiol-052424-082740
Carmen A Mannella, Pawel Swietach, Liron Boyman
{"title":"Calcium Regulation of Mitochondrial Metabolism.","authors":"Carmen A Mannella, Pawel Swietach, Liron Boyman","doi":"10.1146/annurev-physiol-052424-082740","DOIUrl":"10.1146/annurev-physiol-052424-082740","url":null,"abstract":"<p><p>Mitochondrial ATP production dynamically adapts to cellular energy demands, with calcium (Ca2+) playing a crucial regulatory role. In this review, we critically evaluate the evidence for intramitochondrial Ca2+ ([Ca2+]<sub>m</sub>) sensitivity in key energy metabolic pathways, highlighting the [Ca2+]<sub>m</sub> dependence of specific mitochondrial systems. We also address the metabolic consequences of [Ca2+]<sub>m</sub>-sensitive ATP production, particularly its effects on the utilization of specific macronutrients that fuel ATP production. Next, we discuss the primary Ca2+ entry pathway into the matrix, the mitochondrial Ca2+ uniporter (MCU), its macromolecular complex structure (MCUcx), and allosteric regulation by Ca2+. Key to this regulation are specific auxiliary subunits, along with the influence of mitochondrial inner membrane architecture. While the Ca2+ signaling plays an important role, it does not fully explain the scope for regulating ATP production. Emerging evidence suggests that additional signaling systems operating alongside the Ca2+ signaling contribute to the control of mitochondrial ATP production, a topic requiring further investigation.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"393-415"},"PeriodicalIF":19.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145487612","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 Proton-Activated Chloride Channel: Molecular Identification, Structure, and Role in Organelle Physiology. 质子激活的氯离子通道：分子鉴定、结构和在细胞器生理学中的作用。
IF 19.1 1区 医学
Annual review of physiology Pub Date : 2026-02-01 Epub Date: 2025-11-06 DOI: 10.1146/annurev-physiol-022724-105357
Kevin Hong Chen, Tatsuya Hagino, Zhaozhu Qiu
{"title":"The Proton-Activated Chloride Channel: Molecular Identification, Structure, and Role in Organelle Physiology.","authors":"Kevin Hong Chen, Tatsuya Hagino, Zhaozhu Qiu","doi":"10.1146/annurev-physiol-022724-105357","DOIUrl":"10.1146/annurev-physiol-022724-105357","url":null,"abstract":"<p><p>In 2019, a novel membrane protein, PAC (also known as TMEM206), was identified as the long-sought molecular carrier of an acid- or proton-activated chloride current observed ubiquitously in mammalian cells. This discovery has led to rapid progress in revealing its trimetric architecture and biophysical properties, including the pH-sensing mechanism, anion selectivity, and lipid regulation. In addition to the cell surface, the PAC channel predominantly localizes to intracellular organelles (endosomes, phagosomes, and macropinosomes), where it mediates pH-dependent chloride flux to regulate luminal pH and organelle volume. Here, we review these exciting findings and discuss the many aspects of the PAC channel that remain largely unexplored, including its pharmacology, physiological function, and potential role in disease.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"371-391"},"PeriodicalIF":19.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457394","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
From Oil Spills to Air Pollution: The Emergence of Phenanthrene as a Ubiquitous Cardiac Toxicant. 从石油泄漏到空气污染：菲作为普遍存在的心脏毒物的出现。
IF 19.1 1区 医学
Annual review of physiology Pub Date : 2026-02-01 Epub Date: 2025-12-02 DOI: 10.1146/annurev-physiol-042224-093212
Holly A Shiels
{"title":"From Oil Spills to Air Pollution: The Emergence of Phenanthrene as a Ubiquitous Cardiac Toxicant.","authors":"Holly A Shiels","doi":"10.1146/annurev-physiol-042224-093212","DOIUrl":"10.1146/annurev-physiol-042224-093212","url":null,"abstract":"<p><p>Polycyclic aromatic hydrocarbons (PAHs) are released into the environment primarily through industrial processes and the incomplete combustion of organic matter. Their persistence in air, water, and soil facilitates widespread environmental distribution and exposure that directly impact the health of humans, other animals, and ecosystems. In recent years, the 3-ringed PAH phenanthrene has drawn particular interest for its specific cardiotoxicity. Phenanthrene can be transformed in the environment and within the body, leading to metabolites that can also influence heart function. Phenanthrene and its derivatives alter the electrical activity of the heart by inhibiting repolarizing (e.g., <i>I</i> <sub>K</sub>) currents and inhibiting depolarizing (e.g., <i>I</i> <sub>Na</sub> and <i>I</i> <sub>Ca</sub>) currents, which increase the probability of arrhythmias. Phenanthrene and its derivatives also impact cardiac contractility by reducing the amplitude of the intracellular Ca2+ transient in all species examined to date. This review begins by describing the sources and sinks of environmental phenanthrene and how it enters and accumulates within organisms. It then focuses on the potential for, and mechanisms of, modulation of cardiac activity by phenanthrene and its derivatives at the molecular, cellular, intact heart, and whole organism levels. The results provide a comprehensive summary of the propensity of phenanthrene to modulate vertebrate cardiac function, from fish exposed via crude oil to humans breathing polluted air.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"129-154"},"PeriodicalIF":19.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145659989","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
Interrogating Physiological Functions with Light and Chemicals. 用光和化学物质询问生理功能。
IF 19.1 1区 医学
Annual review of physiology Pub Date : 2026-02-01 Epub Date: 2025-11-10 DOI: 10.1146/annurev-physiol-042924-083733
Tianlu Wang, Kai Zhang, Yubin Zhou
{"title":"Interrogating Physiological Functions with Light and Chemicals.","authors":"Tianlu Wang, Kai Zhang, Yubin Zhou","doi":"10.1146/annurev-physiol-042924-083733","DOIUrl":"10.1146/annurev-physiol-042924-083733","url":null,"abstract":"<p><p>Optogenetics and chemogenetics have transformed how physiologists interrogate biological systems by enabling precise control over protein activity and cellular function. Optogenetics uses light-sensitive proteins for rapid and localized control, while chemogenetics employs small molecules to trigger or block specific pathways with systemic and sustained effects. These tools have advanced research in areas such as brain function, heart rhythm, immune response, and gene regulation. They have been applied to disease models that include epilepsy, metabolic and cardiovascular diseases, immunoinflammatory disorders, and cancer. Clinical applications are emerging, such as optogenetic therapies for vision restoration and chemogenetic safety switches in engineered immune cells. In this review, we categorize these tools by their mechanisms of action, compare their advantages and limitations, and discuss strategies to improve their precision, efficiency, and translational capability. As these technologies continue to evolve, they offer powerful approaches to dissect complex physiological processes and drive innovative therapeutic interventions.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"21-46"},"PeriodicalIF":19.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145487675","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
Myeloid Cell Reprogramming and Immune Suppression. 骨髓细胞重编程与免疫抑制。
IF 19.1 1区 医学
Annual review of physiology Pub Date : 2026-02-01 Epub Date: 2025-10-03 DOI: 10.1146/annurev-physiol-050824-111031
Amit Grover, Evgenii N Tcyganov, Dmitry I Gabrilovich
{"title":"Myeloid Cell Reprogramming and Immune Suppression.","authors":"Amit Grover, Evgenii N Tcyganov, Dmitry I Gabrilovich","doi":"10.1146/annurev-physiol-050824-111031","DOIUrl":"10.1146/annurev-physiol-050824-111031","url":null,"abstract":"<p><p>Plasticity of myeloid cells, characterized by their ability to undergo reprogramming in response to environmental cues, is a fundamental feature enabling their versatile functions during immune responses. Macrophages and neutrophils, the primary myeloid cell types, exhibit distinct polarization states. Classical polarization states of macrophages and neutrophils are associated with antimicrobial activity, inflammation promotion, and tissue remodeling. Pathological polarization, observed in chronic inflammation, cancer, and other conditions, is marked by enhanced immune-suppressive activity, aberrant enzymatic activity, and atypical cytokine production, diverging from their classical functions. This review delves into the most up-to-date characterization of those polarization states, the transcriptional and epigenetic factors, and the metabolic pathways governing myeloid cell reprogramming, highlighting the influence of cytokines and tissue-specific conditions, such as hypoxia in tumors, on this process. Understanding the mechanisms underlying the pathological polarization of myeloid cells offers a promising avenue to modulate their activity for targeted therapeutic interventions.</p>","PeriodicalId":8196,"journal":{"name":"Annual review of physiology","volume":" ","pages":"437-457"},"PeriodicalIF":19.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145224803","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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