Physiological Reviews生理学评论
Physiological Reviews(英文缩写 PHYSIOL REV),ISSN 0031-9333,eISSN 1522-1210,中文译名:生理学评论 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 46.513 | Q1 |
| 2022 | 33.600 | Q1 |
| 2023 | 29.900 | Q1 |
| 2024 | 28.700 | Q1 |
| 2025 | 35.700 | Q1 |
Physiological Reviews 最新收录文献
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1. Monocarboxylate Transporters (MCTs) in Physiology and Cancer: from Fundamentals to Clinical Translation.
1. 单羧酸转运蛋白（MCTs）在生理学和癌症中的研究：从基础到临床转化PMID:日期:2026-09-29Monocarboxylate transporters (MCTs) are vital to physiological pH regulation, redox balance, and energy homeostasis by mediating proton-coupled transport of lactate and other monocarboxylates across cell membranes. MCT1 and MCT4 are especially important during metabolically demanding states, where they support lactate shuttling between oxidative and glycolytic cells. To sustain rapid growth and biosynthesis, the metabolism of highly proliferative cells, including cancer cells, shifts toward glycolysis with increased lactate production. In this setting, MCTs enable lactate and proton efflux, preventing intracellular acidification and maintaining glycolytic flux. Cancer cells frequently co-opt this system, overexpressing MCT1 and MCT4, which is associated with aggressive behavior, poor prognosis, and treatment resistance. These insights have motivated the development of MCT inhibitors, one of which has entered early clinical evaluation, suggesting potential therapeutic benefit in selected tumors. This review first introduces core aspects of cellular metabolism and then outlines the physiological roles, regulation, and tissue distribution of MCTs in normal tissues. It next examines how MCTs are dysregulated across cancer types to support the glycolytic phenotype, remodel the tumor microenvironment, and drive malignant progression, with particular focus on the prognostic impact of MCT expression. The article summarizes evidence linking MCT overexpression to poor outcomes and therapy resistance, and surveys efforts to therapeutically target MCTs and key translational barriers. Finally, it highlights future directions for exploiting MCT biology in precision oncology.
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2. Lipid flip-flop in biological membranes: through the lens of TMEM16F.
2. 生物膜中的脂质翻转：通过TMEM16F的视角PMID:日期:2026-09-10The asymmetric distribution of phospholipids between membrane leaflets is a hallmark of all known cells, yet many fundamental questions about membrane lipid asymmetry remain unanswered. Why do cells invest energy to establish and maintain this thermodynamically unstable state? How do cells exploit lipid asymmetry to support essential functions? What are the consequences for health and disease when this organization breaks down? Recent identification of bona fide lipid scramblases, which catalyze rapid phospholipid translocation across the hydrophobic membrane core (lipid flip-flop), has shed new light on these longstanding questions. In particular, studies of the Ca²⁺-activated phospholipid scramblase TMEM16F have revealed how regulated lipid scrambling can couple Ca²⁺ signaling to membrane remodeling, phosphatidylserine (PS) exposure, cellular communication, and disease pathogenesis. In this review, we examine the biology of regulated transmembrane phospholipid flip-flop mediated by lipid scramblases, using TMEM16F as a prototypical model to illustrate core molecular mechanisms, physiological functions, pathological implications, and emerging pharmacological opportunities. By placing TMEM16F within the broader landscape of lipid scramblases and scramblase-like proteins, we highlight how regulated membrane lipid scrambling shapes cell physiology and disease. We also discuss critical knowledge gaps and future directions for understanding this rapidly evolving field.
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3. Understanding physiological adaptations of pregnancy to the chronic hypoxia of high altitude to inform obstetrical and neonatal care.
3. 了解妊娠对高海拔慢性缺氧的生理适应，为产科和新生儿护理提供依据PMID:日期:2026-08-14The chronic hypoxia experienced by high-altitude residents profoundly impacts pregnancy, influencing maternal health, placental function, and the growth and development of the fetus. Exposure to chronic hypoxia during pregnancy increases the risk of complications like preeclampsia and fetal growth restriction and has lasting effects on offspring, extending from infancy to adulthood. Understanding how chronic hypoxia alters physiological adaptations to pregnancy and pregnancy outcomes is essential for high-altitude populations and for gaining broader insights into the mechanisms underlying reduced fetoplacental oxygenation in complicated pregnancy at sea level. This review summarizes current knowledge on physiological adaptations during pregnancy under hypoxic conditions. We describe key studies on the effects of high altitude and chronic hypoxia on pregnancy and examine the maternal, placental, fetal, and long-term physiological consequences. Finally, we review preclinical and clinical studies aimed at identifying interventions that could prevent or alleviate the adverse effects of chronic hypoxia on pregnancy outcomes and beyond.
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4. Extracellular Vesicles in Reproductive Physiology and Pathology.
4. 生殖生理学和病理学中的细胞外囊泡PMID:日期:2026-08-09[中文摘要] 细胞外囊泡（EVs）是脂质包裹的纳米结构，作为双向细胞间通讯的通用介质，在生殖过程中发挥重要作用。EVs在生殖细胞之间转运多种货物，影响配子发生和妊娠等基本生殖过程。在男性生殖道中，附睾体（epididymosomes）和前列腺体（prostasomes）等特化EVs调控精子活化、运动和获能，其中部分作用亦在女性生殖道内发挥。在女性生殖道中，存在于卵泡液、输卵管和子宫中的EVs有助于卵母细胞成熟、受精以及成功着床所必需的胚胎发育和胚胎-母体对话，包括体外受精后。随着妊娠进展，EVs持续在介导母体、胎盘和胎儿各腔室之间的通讯中发挥关键作用，其最终目的是促进免疫耐受和同种异体胎儿的发育。聚焦于人类生殖系统，子痫前期和妊娠期糖尿病等产科疾病的发生以EV释放显著增加和全身性影响为标志，包括内皮功能失调、代谢稳态紊乱和血脑屏障破坏。EV介导信号传导的破坏与生殖病理相关，但具体病因尚未明确。重要的是，EVs为生物标志物发现和治疗应用提供了令人振奋的途径。我们对EVs如何递送其分子货物并影响受体细胞基因表达的理解不断深入，为操控这些过程以及改善不孕症和妊娠并发症的诊断与治疗带来了希望。
[英文摘要] Extracellular vesicles (EVs) are lipid-bound nanostructures that play important roles in reproduction as universal mediators of bidirectional cell-to-cell communication. EVs transfer diverse cargoes between reproductive cells, influencing fundamental reproductive processes such as gametogenesis and pregnancy. In the male reproductive tract, specialized EVs such as epididymosomes and prostasomes regulate sperm activation, motility, and capacitation, exerting some of these effects within the female reproductive tract as well. In the female reproductive tract, EVs found in follicular fluid, oviduct, and uterus aid in oocyte maturation, fertilization, and the vital embryo development and embryo-maternal crosstalk necessary for successful implantation, including after in vitro fertilization. With advancing gestation, EVs continue to play crucial roles in mediating communication between maternal, placental and fetal compartments with the ultimate aim of promoting immunotolerance and development of the allogeneic fetus. Focusing on the human reproductive system, development of obstetric conditions such as preeclampsia and gestational diabetes is marked by a significant increase in EV release and systemic impacts, including endothelial dysregulation, perturbation of metabolic homeostasis and disruption to the blood-brain barrier. Disruption of EV-mediated signaling is linked to reproductive pathologies, but detailed etiologies are not yet defined. Importantly, EVs offer an exciting avenue for both biomarker discovery and therapeutic applications. Our advancing understanding of how EVs deliver their molecular cargo and influence gene expression in recipient cells holds promise for manipulating these processes and improving the diagnosis and treatment of infertility and pregnancy complications.
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5. Manganese transport, homeostasis, and neurotoxicity.
5. 锰的转运、稳态与神经毒性PMID:日期:2026-08-08Manganese (Mn) is an essential metal required for many physiological functions, and deficiency or overexposure is associated with neurological dysfunction and neuropathology. Tight homeostatic control of Mn in the body is required to maintain optimal physiological levels and protect against toxicity. Mn homeostasis has been studied for decades, but there has been limited knowledge of the molecular mechanisms until recently, when the first human genetic disorders of Mn metabolism were described. These discoveries led to the identification of the Mn transporters SLC30A10, SLC39A14, and SLC39A8, which spurred a transformation of research into Mn homeostatic mechanisms. This review provides an overview of Mn physiology and homeostasis and the role of the critical Mn transporters and discusses the progress made within recent years toward understanding how these transporters work together to regulate brain Mn biology under both physiological and pathophysiological Mn conditions.
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6. Long-term potentiation in the brain: A synaptic memory mechanism.
6. 大脑中的长期增强：突触记忆机制PMID:日期:2026-06-27One of the most remarkable properties of the mammalian brain is its ability to change in response to experience, a phenomenon referred to as neural plasticity. Synaptic plasticity specifically refers to activity-dependent changes in synaptic strength or efficacy of synaptic transmission. Synaptic plasticity enables us to acquire and perform different sensory, motor and cognitive tasks, such as playing a musical instrument or learning a language. Synaptic plasticity is involved in the creation of memories and is a phenomenon that varies and evolves over an individual's lifetime. The most extensively studied forms of synaptic plasticity in the mammalian brain are long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission. Sixty years ago, an abstract by Terje Lømo first described a long-lasting synaptic potentiation induced by high-frequency afferent stimulation (1) and seven years later, the first full paper on LTP was published by Tim Bliss and Terje Lømo in The Journal of Physiology (2). Since then, "neuroplasticity" or "brain plasticity" has emerged as a central theme of research in neuroscience. Increasing evidence supports the supposition that LTP is a natural phenomenon that is directly involved in neurodevelopment and learning and memory processes. Additionally, different brain disorders seem to be due to alterations in brain plasticity. Since its discovery, thousands of papers have appeared describing the underlying mechanisms and demonstrating that LTP is a robust and general brain mechanism that exists in animals including humans. Currently, the field is dedicated to defining more precisely the functions in which LTP (and LTD) is involved, including development, learning and memory, as well as their roles in brain disorders. Here, we describe the present state of the field. We foresee tht important discoveries remain to be made with implications for the understanding of, and treatment of, brain disorders.
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7. Catecholamine metabolism revisited: From neurochemistry to integrative physiology and pathophysiology.
PMID:日期:2026-06-26After a previous overview published more than 20 years ago, key aspects of catecholamine metabolism remain incompletely understood by physiologists. Meanwhile, the repertoire of assayable catecholamine-related compounds has expanded. Moreover, alterations in catecholamine metabolic patterns associated with physiological changes, drug effects, and pathophysiological states were not covered; and biochemical phenotyping via kinetic models now makes it possible to elucidate physiology and pathophysiology in individuals. Accordingly, this review starts with the inventory of catecholamine-related compounds and the three main peripheral catecholamine systems (sympathoneuronal, adrenomedullary, and autocrine/paracrine). Catecholamine systems contribute to virtually every organ function, behavior, and emotional state, and we describe situations where alterations in those systems exert syndromic pathophysiological effects. We then describe the relationships of catecholamine metabolic patterns to synthesis, storage, release, reuptake, and intra-neuronal and extra-neuronal metabolism of catecholamines; effects of physiological processes and drugs on those patterns; and catecholamine biochemical patterns associated with pathophysiologic states. We provide examples of how detailed, comprehensive knowledge acquired over the past half century has led to computational models for estimating the rates of processes that characterize specific physiological changes and some clinical disorders. The integrative physiological approach presented here has the potential to pinpoint specific functional abnormalities within catecholaminergic cells and thereby rationalize novel, testable treatment and prevention strategies.
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8. The origins and progression of pyloric metaplasia following gastric mucosal injury.
8. 胃黏膜损伤后幽门化生的起源和进展PMID:日期:2026-06-19The human gastric mucosa contends with insults throughout the course of its normal functions. Superficial injuries are rapidly resolved by the normal cellular lineages within the glandular epithelium. Deeper injuries often cause loss of acid-secreting cells, necessitating extensively coordinated repair mechanisms that significantly alter the cellular content of the gastric glands, culminating in pyloric metaplasia. Pyloric metaplasia is defined by the hyperplastic expansion of foveolar and mucous neck cell lineages as well as spasmolytic polypeptide-expressing metaplasia (SPEM) cells transdifferentiated from zymogenic chief cells. SPEM cells resemble mucus-secreting deep antral gland cells and possess proliferative qualities meant to aid in wound healing. Chief cell transdifferentiation into SPEM cells is regulated by an orderly process in which differentiated zymogenic cells reenter the cell cycle after downregulating mature transcriptional programs. The resolution of injury is followed by the restitution of normal cell lineages. However, metaplasia can persist when there is continuing inflammation and/or severe chronic injury. The aberrant persistence of proliferative SPEM cells can drive glandular intestinalization. The resulting intestinal metaplasia glands, particularly those with mixed gastric and intestinal lineages, are at increased risk for progression to dysplasia and ultimately gastric cancer. Understanding the dynamics of metaplastic cell lineage progression and uncovering lineage transition markers is critical to identifying targets suitable for therapeutic intervention. Here, we discuss the current knowledge, controversies, and remaining questions pertaining to the establishment and progression of metaplasia in response to deep gastric mucosal injury.
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9. AKAP signaling: physiological and pathophysiological roles and opportunities for novel therapeutic concepts.
9. AKAP信号传导：生理和病理生理作用及新型治疗理念的机遇PMID:日期:2026-05-19A-kinase anchoring proteins (AKAPs) received their name based on their ability to bind protein kinase A (PKA). Now, AKAPs have grown to a diverse family of more than 50 proteins, coordinating molecules far beyond PKA and the PKA signaling pathway. AKAPs are scaffolding proteins spanning in size between 15 and several hundred kilodaltons and can directly engage in protein interactions with other signaling proteins, their upstream regulators, and their downstream effectors. AKAPs possess unique targeting domains directing them to defined cellular compartments to coordinate cellular signaling spatially and temporally. A few AKAPs possess their own catalytic activity. AKAPs are crucial in directing cAMP signaling locally and in mediating cross talk with other second messenger systems. This review introduces individual AKAPs and their physiological functions in their respective cellular compartments and illustrates how they organize local signal transduction. The crucial role of AKAPs in coordinating cAMP responses to extracellular cues and how they facilitate specific responses to each stimulus will be exemplified. Dysregulation of AKAPs is associated with or causes disease. We will examine the pathophysiological roles of AKAPs in inherited and noninherited noncommunicable diseases, such as cardiovascular diseases and cancer. Due to the lack of understanding of molecular mechanisms underlying most of these diseases, the available therapeutic approaches often only slow progression and cause side effects. This review will discuss the unique opportunities AKAPs provide to address the medical need for novel therapeutic concepts. Finally, gaps in our knowledge about AKAPs will be outlined, and future directions in AKAP research will be suggested.
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10. Mechanisms of transcranial magnetic brain stimulation.
PMID:日期:2026-05-19Transcranial magnetic stimulation (TMS) noninvasively activates the human cortex through the intact skull and is now employed worldwide to interrogate physiological and pathological functions of the human brain and to treat a variety of neurological and psychiatric brain disorders. Yet the precise routes from the induced electric field to neuronal excitation including network effects remain not fully resolved, limiting the mechanistic basis of all TMS applications. This review deeply surveys how TMS activates the human cortex. We integrate evidence from physics, biophysics, computational modeling, neurophysiological studies in humans using electromyography, electroencephalography, and epidural spinal recordings, and converging nonhuman primate, rodent, and cortical slice studies. Collectively, the data suggest that TMS preferentially depolarizes superficial large-diameter myelinated axons, likely at bends, thereby triggering near-instantaneous synaptic activation of local cortical circuits and the emergence of long-range corticocortical and cortico-subcortical network activity. Through this cascade, axonal excitation, cell and circuit recruitment, and network propagation, TMS provides a versatile probe of excitability, function, and dysfunction across spatial scales, from single axons to distributed human brain networks.