PHYSIOLOGY生理学
PHYSIOLOGY(英文缩写 PHYSIOLOGY),ISSN 1548-9213,eISSN 1548-9221,中文译名:生理学 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 | 11.846 | Q1 |
| 2022 | 8.400 | Q1 |
| 2023 | 5.300 | Q1 |
| 2024 | 10.300 | Q1 |
| 2025 | 14.600 | Q1 |
PHYSIOLOGY 最新收录文献
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1. Physiopathology of PMOS from a Neuroendocrine Perspective.
1. 从神经内分泌角度看PMOS的病理生理学PMID:日期:2026-09-29Polyendocrine metabolic ovarian syndrome (PMOS) is the most common reproductive and cardiometabolic disorder in women of reproductive age. Once viewed as primarily an ovarian disease, it is now recognized as a neuroendocrine-metabolic disorder driven by dysregulation of the hypothalamic-pituitary-gonadal axis. A central feature of the syndrome is increased gonadotropin releasing hormone (GnRH) pulsatility, which drives excess luteinizing hormone (LH) secretion, disrupts the LH/follicle stimulating hormone (FSH) balance, and promotes ovarian androgen excess and anovulation. Hypothalamic Kisspeptin neurons, the principal regulators of GnRH pulse generation, show altered activity and impaired steroid feedback sensitivity. Anti-Müllerian hormone (AMH) has emerged as an ovary-to-brain signal that directly stimulates GnRH neurons and remodels the neuroendocrine interface, amplifying LH secretion and perpetuating reproductive dysfunction. Developmental programming, through interactions among genetic, environmental, and epigenetic factors, may durably alter the organization and function of hypothalamic circuits, predisposing to neuroendocrine dysfunction later in life. In parallel, metabolic dysfunction, including insulin resistance and adipose tissue dysfunction, can interact bidirectionally with reproductive and neuroendocrine pathways, reinforcing hyperandrogenism and perturbing both reproductive and energy homeostasis. This review summarizes current knowledge of the neuroendocrine mechanisms underlying PMOS and discusses emerging targeted therapies that may offer disease-modifying approaches for this prevalent and heterogeneous disorder.
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2. Cellular and molecular mechanisms of muscle spindle development and function.
PMID:日期:2026-09-02An organism's external environment is dynamic and ever-changing. Survival depends on an animal's ability to engage with its surroundings through adaptive and purpose driven movement. Organisms that rely on such movement are endowed with an internal sensory system, known as proprioception, which enables the precise detection and awareness of the body and its limbs in space. The principal receptors that give rise to this system are known as "proprioceptors", a unique population of peripheral sensory neurons embedded within skeletal muscle and tendons, referred to as muscle spindles and Golgi tendon organs, respectively. Over the years, advancements in cellular, molecular, and electrophysiological techniques have provided fundamental insight into the signaling pathways that regulate proprioceptor development. These same approaches have also facilitated the discovery of the ionic and neuromodulator mechanisms that regulate proprioceptor activity. In more recent years, emerging evidence suggests that proprioceptive feedback may engage in non-cell autonomous regulation of other physiological systems, potentially expanding their role beyond detectors of movement and force. In this review, we will examine the cellular and molecular mechanisms that govern the development and function of muscle spindle afferents. Furthermore, we will highlight their emerging influence on neurological and musculoskeletal disease.
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3. Cardiac Protein Palmitoylation: Mechanisms, Functions, and Therapeutic Potential.
3. 心脏蛋白棕榈酰化：机制、功能与治疗潜力PMID:日期:2026-08-28Protein S-palmitoylation is a reversible lipid modification which regulates the localisation, stability, and activity of a substantial fraction of the proteome. In the heart S-palmitoylation controls the function of membrane proteins which regulate cardiac excitability and contractility. Recent work has moved the S-palmitoylation field beyond descriptive cataloguing towards mechanistic understanding, revealing how site-specific S-palmitoylation can modulate protein structure and function in a precise and quantifiable manner. These advances position S-palmitoylation as a tuneable regulator of cardiac proteins and consequently cardiac function, and a potential target for therapeutic modulation. In this review, we focus on the role of S-palmitoylation in cardiac function, highlighting its effects on key ion channels and transporters, including CaV1.2, NaV1.5 and NCX1, and the resulting consequences for cardiac electrophysiology and calcium handling. We also discuss emerging experimental tools and strategies to selectively manipulate S-palmitoylation and their limitations. Finally, we consider the translational potential of targeting S-palmitoylation, emphasising the need for selective intervention strategies informed by detailed molecular and structural insight.
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4. Non-neuronal acetylcholine: from cellular signaling to clinical implications.
4. 非神经元乙酰胆碱：从细胞信号传导到临床意义PMID:日期:2026-08-21For over a century, acetylcholine (ACh) was viewed primarily as a wired neurotransmitter of cholinergic nerves. However, accumulating evidence supports the view of the non-neuronal cholinergic system (NNCS) as an evolutionarily ancient autocrine and paracrine network operating across peripheral tissues. Rather than an extension of neuronal signaling, non-neuronal ACh can be viewed as a tissue-embedded chemical communication system positioned at the interface of cellular homeostasis and systemic neural reflexes. This review frames the NNCS as a network of tissue-resident ACh-producing cells that operates through mechanisms distinct from autonomic neural circuits. Across cardiovascular, immune, epithelial, metabolic, reproductive, and renal systems, NNCS signaling couples local cues to adaptive cellular responses. In the endothelium, ACh translates shear stress into M3 receptor-driven Ca2+ oscillations, endothelial nitric oxide synthase activation, and flow-mediated dilation, with indirect readouts of vascular cholinergic-nitric oxide coupling. In inflammatory and metabolic niches, macrophage-derived ACh regulates adipose tissue inflammation, supports peritoneal macrophage efferocytosis, and engages α7 nicotinic receptor pathways implicated in organ protection. At mucosal surfaces, brush/tuft cell signaling contributes to chemosensation, mucociliary clearance, luminal ACh release, anti-helminth immunity, and gut-brain communication. Non-neuronal ACh also modulates gametogenesis, placental transport, embryonic development, stem cell fitness, and conserved developmental mechanisms in honeybees. The kidney provides an informative example of layered regulation, where podocyte-derived ACh and tubular cholinergic receptor signaling are distinguished from vagus-spleen renal protective pathways and pelvic parasympathetic afferents regulating blood pressure. Finally, we address outstanding questions regarding ACh release, extracellular stability, spatial range, biomarkers, and tissue-selective therapeutic targeting.
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5. Respiratory control dysfunction and vulnerability in Parkinson's disease.
PMID:日期:2026-08-18Respiratory dysfunction is increasingly recognized as a clinically relevant yet underexplored feature of neurodegenerative diseases, particularly Parkinson's disease (PD). Although traditionally defined by motor symptoms resulting from dopaminergic degeneration, PD also affects neural systems involved in autonomic and respiratory control. Clinical and experimental evidence demonstrates that respiratory impairments in PD include alterations in respiratory rhythm generation, chemosensitivity, ventilatory responses to hypoxia and hypercapnia, and sleep-related breathing regulation. Emerging data indicate that these disturbances are not merely secondary consequences of motor dysfunction, but instead reflect selective vulnerability of brainstem respiratory networks. In this review, we discuss current evidence from human studies and experimental models, with emphasis on circuit-level mechanisms underlying respiratory dysfunction in PD. We highlight how oxidative stress, neuroinflammation, and neuromodulatory alterations contribute to degeneration and dysfunction of respiratory-related nuclei. We further examine the complex interactions between chemosensory control, sleep-wake regulation, and respiratory stability, as well as compensatory mechanisms that may partially preserve ventilatory function during disease progression. Finally, we discuss potential treatments for these dysfunctions, as well as major conceptual gaps and controversies in the field, including species-dependent differences, limitations of current experimental models, and challenges in translating mechanistic findings into clinical interventions. We propose that respiratory control networks represent a mechanistically relevant and selectively vulnerable system in PD, with important implications for early diagnosis, biomarker discovery, and the development of targeted therapeutic strategies.
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6. Physiological Limits and Climate Vulnerability in Tropical Freshwater Fishes.
PMID:日期:2026-08-11Tropical freshwater fishes evolved under historically stable thermal, oxygen, and chemical regimes that favored physiological specialization within narrow environmental ranges. Rapid climate warming is now compressing these already limited safety margins by simultaneously increasing metabolic demand, reducing oxygen availability, altering ionoregulatory balance, and intensifying exposure to pollutants. Evidence from Amazonian systems shows that physiological limits emerge from interacting constraints rather than single stressors, and that tolerance measured under controlled conditions often overestimates persistence in nature. As safety margins erode, energetic trade-offs propagate from molecular stress and metabolic disruption to impaired growth, reproduction, and population stability, ultimately altering ecosystem function. This integrative perspective reveals that vulnerability is defined not by absolute thermal limits alone, but by how multiple constraints accumulate and scale across levels of biological organization. Understanding these scaling relationships is essential for predicting resilience and for advancing physiology from documenting responses toward anticipating ecological outcomes in a rapidly warming world.
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7. Two Pulses Per Beat: Parallel Energetics of Myocardium and Coronary Wall.
PMID:日期:2026-07-23Each heartbeat is initiated by a sinoatrial node action potential that propagates through the myocardial syncytium, triggering sequential contraction of the four chambers and propelling blood through the coronary, pulmonary, and systemic circulations. This mechanical event is fueled by two coupled energetic pulses: one in the working myocardium, where ATP is consumed by Ca cycling, cross-bridge cycling and ion pumping, and a second in the coronary vascular wall, where smooth muscle cells (SMCs), endothelial cells, and pericytes expend ATP to maintain tone, manage Ca, and coordinate perfusion against systolic compression that arrests their blood supply. Cardiac myocytes and coronary SMCs share the same actomyosin machinery but are activated differently. In myocytes, beat-to-beat Ca transients drive Ca binding to troponin C to permit synchronous contraction; in coronary SMCs, Ca/calmodulin activates myosin light-chain kinase (MLCK), which phosphorylates myosin to sustain tone. In both cell types, ATP availability sets the ceiling on excitability: when the energetic budget is met, ion pumps, SERCA, and ATP-sensitive channels operate within range and electrical behavior is stable; when it is not, excitability fails. Biosensor measurements reveal beat-to-beat ATP gains and dips in sinoatrial node and ventricular myocytes across systole and diastole. The vascular wall undergoes its own synchronous cycle: systolic compression arrests perfusion while MLCK, SERCA, and Kir2.1-mediated retrograde signaling compete for a diastolic replenishment window that narrows with each heart-rate increment. We propose that cardiac energetics must treat these pulses as co-equal, reframing heart failure as a vascular and computational disease of the coronary wall.
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9. Dietary modulation of CMA: implications for cancer prevention and therapy.
9. CMA的饮食调节：对癌症预防和治疗的意义PMID:日期:2026-07-18Chaperone-mediated autophagy (CMA) is a selective lysosomal degradation pathway that links nutrient availability to intracellular proteostasis through the targeted turnover of selective cytosolic proteins. Through this selective control of protein quality, CMA participates in the regulation of metabolic adaptation, cellular homeostasis, and stress responses. CMA is highly responsive to nutritional cues, including caloric restriction (CR), fasting, and changes in macronutrient composition, positioning this pathway as a key mediator of cellular adaptation to metabolic stress. In cancer, CMA displays context-dependent functions that influence tumor metabolism, genomic stability, and survival under adverse microenvironmental conditions. These dual roles suggest that dietary modulation of CMA may shape tumor initiation and progression through effects on cellular proteostasis and metabolic plasticity. In this review, we summarize current knowledge on the molecular mechanisms by which nutritional signals regulate CMA and discuss the physiological implications of nutrition-driven CMA modulation for cancer prevention and therapy.
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10. Evolution of Adaptive Non-Shivering Thermogenesis in Mammals.
10. 哺乳动物适应性非颤抖性产热的演化PMID:日期:2026-06-29Endothermy depends on the ability to generate heat beyond basal metabolic output. The transition from incidental metabolic heat production to regulated adaptive thermogenesis represents a critical, yet poorly understood milestone in vertebrate evolution. In vertebrates, adaptive thermogenesis includes shivering thermogenesis and non-shivering thermogenesis (NST), the latter involving molecular mechanisms that release energy in the form of heat independently of muscle contraction. This review synthesizes physiological, comparative, and evolutionary findings on adaptive NST, with a focus on adipose-based thermogenesis mediated by its unique mitochondrial uncoupling protein 1 (UCP1). We highlight a two-stage evolutionary model in which a pre-thermogenic adipose program governing UCP1 expression preceded the emergence of efficient UCP1-mediated thermogenesis in eutherian mammals. The source of NST and underlying mechanisms in other tissues and in non-eutherian endothermic vertebrates are less well understood. We discuss proposed UCP1-independent sources of cellular heat production in adipose tissue and muscle. Although these pathways can increase cellular energy expenditure, evidence supporting their role as dedicated and regulated thermogenic mechanisms remains limited to date. Collectively, these findings suggest that adaptive NST is not a singular conserved mechanism but a diverse and context dependent evolutionary strategy with important implications for understanding human physiology and disease.