JOURNAL OF PHYSIOLOGY-LONDON
JOURNAL OF PHYSIOLOGY-LONDON(英文缩写 J PHYSIOL-LONDON),ISSN 0022-3751,eISSN 1469-7793 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 | 6.228 | Q1 |
| 2022 | 5.500 | Q1 |
| 2023 | 4.700 | Q1 |
| 2024 | 4.400 | Q1 |
| 2025 | 4.600 | Q1 |
JOURNAL OF PHYSIOLOGY-LONDON 最新收录文献
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1. Cancer-associated fibroblast heterogeneity across solid and haematological malignancies: Lessons from colorectal cancer and multiple myeloma.
1. 实体瘤与血液恶性肿瘤中癌症相关成纤维细胞的异质性：来自结直肠癌和多发性骨髓瘤的启示PMID:DOI:日期:2026-10-05Although substantial advances have been made in cancer immunotherapy, the immunosuppressive tumour microenvironment (TME) continues to pose a significant obstacle to the achievement of sustained clinical responses. Cancer-associated fibroblasts (CAFs) are increasingly recognised as pivotal regulators in the TME. Their functional adaptability shapes immune responses through extracellular matrix (ECM) remodelling, metabolic reprogramming and the secretion of immunomodulatory factors. This review explores the heterogeneity and plasticity of CAFs, characterising them as dynamic functional states, including myofibroblastic (myCAF), inflammatory (iCAF), antigen-presenting (apCAF) phenotypes and hypoxia-induced senescent fibroblasts (hsCAF), which transition fluidly in response to microenvironmental cues and oncogenic signalling. Through a comparative analysis of colorectal cancer (CRC) and multiple myeloma (MM), this review highlights how stromal regulation is adaptive across solid and haematological malignancies. In CRC, CAFs establish dense, collagen-rich ECM barriers that exclude effector T cells, whereas, in MM, they establish adhesion-dependent niches within the bone marrow to spatially segregate immune cells from malignant plasma cells. This review also discusses how oncogenic drivers such as KRAS and TP53 'educate' the stromal microenvironment and explores emerging immune evasion mechanisms, including the sialic acid-Siglec glyco-immune checkpoint. Current therapeutic approaches are shifting from non-selective stromal depletion toward normalising phenotypes, blocking secretome factors and disrupting metabolic interactions. The integration of spatial multi-omics and artificial intelligence provides a framework for mapping these functional landscapes. In conclusion, harnessing CAF heterogeneity in multimodal combination therapies may help shift the tumour microenvironment from an immunosuppressive to a more pro-immune state.
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3. {"_":"Large-conductance calcium-activated potassium (BK) channels regulate respiratory, metabolic and behavioural responses to CO/pH in mice.","sub":["2"]}
3. 大电导钙激活钾（BK）通道调控小鼠对CO/pH的呼吸、代谢和行为反应PMID:DOI:日期:2026-10-02Large-conductance Ca-activated K (BK) channels regulate excitability across physiological systems, and BK channelopathies cause neurodevelopmental delay, cognitive disability and structural brain malformations. The firing rate response of CO/pH chemosensitive neurones has been suggested to be modulated by the BK channels' activity, which would function as a 'brake' on the chemosensitive response. Thus, our study examined the role of BK channels in ventilatory, metabolic and behavioural responses under normocapnic and hypercapnic conditions in wild-type (Slo1) and BK channel knockout (Slo1) mice of both sexes during postnatal development. Additionally, the electrophysiological properties and chemosensitivity of locus coeruleus (LC) neurones in Slo1 and Slo1 mice of both sexes were studied. Our data show that Slo1 mice displayed multiple changes in respiratory and behavioural phenotypes. Across sexes, Slo1 animals experienced a higher rate of apnoeic events: females exhibited more spontaneous apnoeas, whereas males showed more post-sigh apnoeas and sighs. Slo1 males also demonstrated an exaggerated chewing reflex. Behaviourally, Slo1 females spent less time in the periphery and more time in the centre of the open-field arena compared with wild-type females. During the panic-inducing 20% CO challenge, both sexes showed reduced defensive responses, including fewer escape jumps. Lastly, LC neurones from Slo1 males exhibited an enhanced chemosensitive response to CO compared with controls. These findings demonstrate that loss of BK channels disrupts respiratory stability, alters behavioural responses and enhances central CO chemosensitivity in an age- and sex-dependent manner. KEY POINTS: Absence of BK channels increases breathing variability and apnoea events during postnatal development. BK channel deletion leads to an augmented hypercapnic ventilatory response during postnatal development in a sex-dependent manner. Loss of BK channels reduces panic-like behavioural responses during panic attack induction. LC neurones lacking BK channels exhibit increased CO chemosensitivity in male mice.
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4. From in silico to in vivo: The possibilities and limitations of systems modelling in understanding age-associated anabolic resistance.
4. 从计算机模拟到体内实验：系统建模在理解与年龄相关的合成代谢抵抗中的可能性和局限性PMID:DOI:日期:2026-10-02该文献暂无摘要。
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5. Myocardial stretch-induced ROS production is enhanced prior to the development of heart failure under TAC-induced pressure overload.
PMID:DOI:日期:2026-10-01Acute myocardial stretch induces reactive oxygen species (ROS) production via NADPH oxidase 2 (NOX2), referred to as stretch-induced ROS. Recently, we demonstrated that stretch-induced ROS serves as a physiological signal in the heart, facilitating calcium release from ryanodine receptors to maintain contractility against acute mechanical load. Chronic mechanical overload triggers oxidative stress, leading to cardiac remodelling and heart failure. Although both conditions are mechanically induced, the relationship between physiology and pathophysiological ROS production remains unclear. To address this issue, we investigated changes in stretch-induced ROS production during the development of transverse aortic constriction (TAC)-induced heart failure in wild-type (WT-TAC) and NOX2 knockout (NOX2 KO-TAC) mice. At 2 weeks post-TAC, no significant differences were observed in basal ROS levels or cardiac function between the two groups, and cardiac remodelling was evident in neither group. However, stretch-induced ROS production was significantly increased in the WT-TAC group. At 5 weeks post-TAC, the WT-TAC group progressed to heart failure, reduced ejection fraction with remodelling accompanied by increased basal ROS levels, while no progression was observed in the NOX2 KO-TAC group. The present study demonstrated that in TAC-induced heart failure, physiological acute stretch-induced ROS production increases prior to the elevation of oxidative stress. This suggests that the enhancement of physiological stretch-induced ROS levels in response to chronic pressure overload may induce excessive ROS production, contributing to heart failure. Therefore, pathological oxidative stress may originate from the physiological stretch-induced ROS production pathway. KEY POINTS: Myocardial acute stretch-induced reactive oxygen species (ROS) serves as a physiological signal in the heart, while chronic mechanical overload triggers pathological oxidative stress. Although both conditions are mechanically induced, the relationship between physiology and pathophysiological ROS production remains unclear. We investigated changes in stretch-induced ROS and oxidative stress during the development of pressure overload-induced heart failure using transverse aortic constriction (TAC). TAC-induced chronic pressure overload enhanced physiological acute stretch-induced ROS production prior to the development of oxidative stress and heart failure. The results suggest that pathological oxidative stress in mechanical overload-induced heart failure may originate from physiological acute stretch-induced ROS.
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6. Tendon-cy to differ: Protein synthesis in healthy and tendinopathic tendon.
6. 易患肌腱病的倾向：健康肌腱与肌腱病肌腱中的蛋白质合成PMID:DOI:日期:2026-09-29该文献暂无摘要。
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7. {"_":"Macrophage-derived CD38 mediates colitis through NAD depletion.","sup":["+"]}
7. {"_":"巨噬细胞来源的CD38通过NAD耗竭介导结肠炎。","sup":["+"]}PMID:DOI:日期:2026-09-29Colitis, a chronic inflammatory bowel disease (IBD), is pathologically linked to immune dysregulation; however, the contribution of cellular metabolic alterations to its pathogenesis remains incompletely understood. In this study, untargeted metabolomic analysis revealed marked disruption of NAD metabolism, accompanied by increased expression of CD38, a major NAD-glycohydrolase, in colitis. Restoring NAD levels through supplementation with its precursors or pharmacological inhibition of CD38 activity effectively alleviated the pathological symptoms of colitis. Mechanistically, colitis induced a pronounced upregulation of CD38 specifically in macrophages. Myeloid-specific deletion of Cd38 significantly attenuated both metabolic disturbances and inflammatory responses associated with colitis. These findings identify macrophage CD38 as a critical regulator of intestinal inflammation and highlight the CD38/NAD axis as a potential therapeutic target for IBD. KEY POINTS: Altered NAD metabolism is closely associated with intestinal inflammation, yet the specific cellular mechanisms contributing to this decline remain to be fully elucidated. By supplementing with nicotinamide mononucleotide or inhibiting the enzyme CD38 that consumes NAD with drugs, the NAD level can be effectively restored, which can alleviate the colitis induced by dextran sulphate sodium to a certain extent. During intestinal inflammation, the upregulation of CD38 is predominantly driven by infiltrating macrophages. Myeloid-specific deletion of CD38 preserves NAD homeostasis and ameliorates colitis, highlighting its essential role in disease progression. Targeting macrophage CD38 establishes a key regulatory link between NAD metabolism and intestinal inflammation, providing a potential therapeutic strategy for inflammatory bowel diseases.
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8. Calcium-activated chloride channels in smooth muscle organs: The ANO1 and only……?
8. 平滑肌器官中的钙激活氯通道：ANO1及其唯一……？PMID:DOI:日期:2026-09-27该文献暂无摘要。
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9. Effects of exercise followed by a low-carbohydrate diet on peak fat oxidation and mitochondrial coupling control and efficiency in healthy trained men.
9. 运动后进行低碳水化合物饮食对健康受过训练男性峰值脂肪氧化及线粒体偶联控制与效率的影响PMID:DOI:日期:2026-09-27Whole-body fat oxidation correlates with mitochondrial oxidative capacity, emphasizing the role of mitochondrial function in systemic and skeletal muscle substrate utilization during exercise - a relationship that may be modulated by the prevailing fuel availability. Muscle glycogen is an important fuel during exercise due to its effects on substrate metabolism, but its influence on peak fat oxidation (PFO) and mitochondrial coupling control and efficiency (MCCE) remains unclear. The aim of the study was to investigate the influence of muscle glycogen content on PFO, the intensity eliciting PFO (Fat) and MCCE. Ten trained men participated in a randomized crossover study comprising two interventions conducted over two consecutive days. Day 1 included anthropometric assessments, blood sampling, a muscle biopsy and a graded exercise test followed by a glycogen depletion protocol. The following day blood sampling, muscle biopsy and the graded exercise test were repeated. A diet high or low in carbohydrate was consumed between the days to manipulate glycogen levels. The experiment was repeated after 7-14 days. Muscle samples were analysed for glycogen and triacylglycerol content and MCCE. PFO increased after both interventions and was further enhanced by the combined exercise and low-carbohydrate intervention, where muscle glycogen was low. Fat increased only following the combined exercise and low-carbohydrate intervention. MCCE was unaffected by the interventions. The study concludes that exercise-induced glycogen depletion together with a low-carbohydrate diet increases PFO and Fat but does not influence MCCE. These findings have implications towards understanding and optimizing fat oxidation and as a potential read out of metabolic flexibility. KEY POINTS: Whole-body fat oxidation is linked to mitochondrial capacity, yet the role of endogenous fuel availability in this relationship has not been studied. Muscle glycogen is a primary exercise fuel, but its specific influence on peak fat oxidation (PFO), the exercise intensity that elicits PFO (Fat) and mitochondrial coupling control and efficiency (MCCE) is unclear. Ten trained men completed a randomized crossover study using glycogen depletion and dietary intervention to alter glycogen levels, with exercise tests and muscle biopsies performed at baseline and postintervention. Exercise-induced glycogen depletion combined with a low-carbohydrate diet increased both PFO and Fat, whereas there was no effect on MCCE. These findings clarify the regulation of PFO and the combined effect of exercise-induced glycogen depletion and low carbohydrate diet, and that this is not regulated through changes in mitochondrial function.
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10. Human placental transfer of xenobiotics in health and disease: New approach methodologies for developmental and reproductive toxicology testing and mathematical modelling.
10. 健康和疾病状态下人体胎盘对外源物质的转运：发育与生殖毒理学检测及数学建模的新方法PMID:DOI:日期:2026-09-26This review addresses an important and timely topic at the intersection of placental biology with respect to barrier transfer kinetics, toxicology and mathematical modelling in the context of emerging regulatory drivers to reduce and replace animal use in developmental and reproductive toxicology (DART) testing. The scope of this review is to provide a comprehensive overview of (i) placental structure and function across gestation, (ii) human-specific transfer mechanisms for nutrients and xenobiotics, (iii) ex vivo and in vitro human placental models, (iv) mathematical and computational modelling frameworks for placental transfer and (v) pathological influences on transfer kinetics. It aims to serve as a reference for physiologists, toxicologists and placental modelling specialists within the rapidly evolving field of non-animal technologies for DART testing.