Current Opinion in Physiology最新文献

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The role of epicardial fat in the progression of cardiovascular disease in women 心外膜脂肪在女性心血管疾病进展中的作用

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-12-10 DOI: 10.1016/j.cophys.2025.100888

Ruzzell C Flores, Erele Tzidon, Inna Rabinovich-Nikitin

Obesity is a global health burden with significant sex-specific implications, especially in cardiovascular disease (CVD). Epicardial fat tissue (EFT), a metabolically active visceral fat depot between the myocardium and visceral pericardium, plays a critical role in cardiac health. Under normal conditions, EFT supports the heart via anti-inflammatory signaling, fatty acid metabolism, and nitric oxide–mediated vasodilation. However, in obesity and cardiometabolic syndrome, EFT becomes proinflammatory, contributing to cardiac remodeling and endothelial dysfunction. Since women experience unique hormonal and metabolic influences, risk factors such as menopause, polycystic ovarian syndrome, vitamin D deficiency, and sleep apnea are linked to increased EFT in women, independent of body mass index, and correlate with adverse cardiac remodeling and inflammation. Therapeutic strategies such as exercise, GLP-1 receptor agonists, and hormone replacement therapy show promise in reducing EFT. Understanding sex-specific EFT biology is essential for personalized CVD prevention and treatment in obesity-related disorders.

肥胖是一种全球性的健康负担，具有显著的性别特异性影响，特别是在心血管疾病（CVD）中。心外膜脂肪组织（EFT）是介于心肌和心包之间的代谢活跃的内脏脂肪库，在心脏健康中起着至关重要的作用。在正常情况下，EFT通过抗炎信号、脂肪酸代谢和一氧化氮介导的血管舒张来支持心脏。然而，在肥胖和心脏代谢综合征中，EFT变成促炎，导致心脏重塑和内皮功能障碍。由于女性经历了独特的激素和代谢影响，绝经、多囊卵巢综合征、维生素D缺乏和睡眠呼吸暂停等风险因素与女性EFT增加有关，独立于体重指数，并与不良的心脏重塑和炎症相关。运动、GLP-1受体激动剂和激素替代疗法等治疗策略有望减少EFT。了解性别特异性EFT生物学对于肥胖相关疾病的个性化CVD预防和治疗至关重要。

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Sex-based differences in outcomes after coronary artery bypass graft surgery 冠状动脉搭桥术后结果的性别差异

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-12-10 DOI: 10.1016/j.cophys.2025.100889

Alice Narushevich , Yazan Saleh , Abigail Greek , Hamnah Majeed , Bobby Yanagawa

Coronary artery bypass graft (CABG) surgery is the gold standard treatment for complex coronary revascularization. Despite advancements in the field, females continue to experience higher rates of morbidity and mortality post-CABG surgery compared to males. Such differences may be explained by smaller coronary anatomy, technically more challenging surgery, delayed diagnosis leading to a more complex disease process at presentation, different use of surgical techniques, and the under-representation of females in cardiac surgery. Potential targeted strategies to improve surgical outcomes in females post-CABG surgery may include the creation of specialized clinics focused on female cardiovascular health, clinical trials that focus on recruitment of female participants in the primary analysis, and increased female physician representation in cardiac surgery. This narrative review provides an in-depth summary of sex-based differences in CABG surgery outcomes, with a focus on the most recent published literature.

冠状动脉搭桥（CABG）手术是复杂冠状动脉重建术的金标准治疗。尽管该领域取得了进步，但女性在cabg手术后的发病率和死亡率仍然高于男性。这种差异可能是由于冠状动脉解剖结构较小，手术技术上更具挑战性，诊断延迟导致更复杂的疾病过程，不同的手术技术使用，以及女性在心脏手术中的代表性不足。改善女性冠状动脉搭桥术后手术结果的潜在目标策略可能包括：建立专注于女性心血管健康的专门诊所，在初步分析中重点招募女性参与者的临床试验，以及增加女性医生在心脏手术中的代表性。这篇叙述性综述深入总结了基于性别的CABG手术结果差异，重点是最近发表的文献。

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Unraveling the role of the pulmonary renin–angiotensin system in inflammatory lung injury and hypertension 揭示肺肾素-血管紧张素系统在炎性肺损伤和高血压中的作用

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-11-28 DOI: 10.1016/j.cophys.2025.100876

Chuanming Xu , Ying Zhu , Mengzhi Zhu

Inflammatory lung injury involves pulmonary renin–angiotensin system (RAS) imbalance, manifested as excessive activation of the ACE/AngII/AT₁R axis and reduced activity of the ACE2/Ang/1–7/MasR axis. This imbalance may serve as an important bridge connecting hypertension and inflammatory lung injury. Multiple pathological conditions, including respiratory virus infections, acute lung injury, acute respiratory distress syndrome, chronic obstructive pulmonary disease, and idiopathic pulmonary fibrosis, activate the ACE/AngII/AT₁R axis and inhibit the ACE2/Ang/1–7/MasR axis in the lungs. Restoring dual-axis balance reduces blood pressure and mitigates inflammatory lung injury, making the pulmonary RAS a promising therapeutic target. This review outlines the existing evidence regarding the role of pulmonary RAS in the context of inflammatory lung injury and hypertension, emphasizing mechanistic insights and potential therapeutic implications.

炎性肺损伤涉及肺肾素-血管紧张素系统（RAS）失衡，表现为ACE/AngII/AT1R轴过度激活，ACE2/Ang/ 1-7 /MasR轴活性降低。这种不平衡可能是连接高血压和炎症性肺损伤的重要桥梁。呼吸道病毒感染、急性肺损伤、急性呼吸窘迫综合征、慢性阻塞性肺疾病、特发性肺纤维化等多种病理情况可激活肺内ACE/AngII/AT1R轴，抑制肺内ACE2/Ang/ 1-7 /MasR轴。恢复双轴平衡可降低血压，减轻炎性肺损伤，使肺RAS成为一个有希望的治疗靶点。本文概述了关于肺RAS在炎症性肺损伤和高血压中的作用的现有证据，强调了其机制和潜在的治疗意义。

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Circadian physiology changes with aging: age is just a number, but circadian physiology keeps time 生理昼夜随着年龄的增长而变化：年龄只是一个数字，但生理昼夜保持着时间

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-11-21 DOI: 10.1016/j.cophys.2025.100875

Natalie J Bohmke, Karyn A Esser

Circadian rhythms are inherent cycles of physiology and behavior that occur over approximately 24 h and are modulated by the cell-autonomous molecular clock. The molecular clocks throughout the body are aligned by the suprachiasmatic nucleus to contribute to robust daily variation of physiology, including core temperature, blood pressure, and heart rate. Alterations to the alignment of circadian clocks and changes to circadian rhythms of behavior and physiological processes are contributors to parameters that impact health and disease. In this review, we summarize what is known about changes to circadian rhythms of human behavior and physiology during older adulthood and the opportunities for future investigation of circadian physiology in older adults.

昼夜节律是生理和行为的固有周期，发生在大约24小时内，由细胞自主分子钟调节。整个身体的分子钟由视交叉上核排列，以促进生理的日常变化，包括核心温度、血压和心率。改变生物钟的排列和改变行为和生理过程的昼夜节律是影响健康和疾病的参数的贡献者。在这篇综述中，我们总结了人类行为和生理昼夜节律在老年期的变化，以及未来研究老年生理昼夜节律的机会。

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Unlocking therapies for neurodegeneration: targeting mitochondrial dysfunction and oxidative stress in Alzheimer’s disease 解锁神经退行性疾病的治疗：针对阿尔茨海默病的线粒体功能障碍和氧化应激

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-11-20 DOI: 10.1016/j.cophys.2025.100874

Jia Hui Wong, Kei Onn Lai, Anna M Barron

Alzheimer’s disease (AD) arises not only from protein aggregates but also from a breakdown in cellular energy and redox balance. Early mitochondrial defects cause excess reactive oxygen species, undermining neuronal synapses, while microglia shift into a glycolysis-driven, proinflammatory state that hinders amyloid clearance. Cutting-edge imaging and single-cell profiling now reveal these metabolic derangements before hallmark plaques emerge. This review synthesizes recent insights into mitochondrial oxidative stress, microglial metabolic reprogramming, and neurovascular redox imbalance, highlighting evidence that restoring mitochondrial function improves disease outcomes. We also examine how artificial intelligence accelerates the identification of oxidative-stress biomarkers and mitochondria-targeted therapeutics through integrative analyses of omics, imaging, and clinical datasets. Together, these mechanistic and computational advances point toward mitochondria-centered, data-driven strategies for precision therapy and early intervention in AD.

阿尔茨海默病（AD）不仅源于蛋白质聚集，还源于细胞能量和氧化还原平衡的破坏。早期线粒体缺陷导致活性氧过剩，破坏神经元突触，同时小胶质细胞转变为糖酵解驱动的促炎状态，阻碍淀粉样蛋白的清除。在标志性斑块出现之前，先进的成像和单细胞分析现在揭示了这些代谢紊乱。这篇综述综合了线粒体氧化应激、小胶质细胞代谢重编程和神经血管氧化还原失衡的最新见解，强调了恢复线粒体功能改善疾病结局的证据。我们还研究了人工智能如何通过组学、成像和临床数据集的综合分析加速氧化应激生物标志物和线粒体靶向治疗的识别。总之，这些机制和计算上的进步指向了以线粒体为中心、数据驱动的精准治疗和AD早期干预策略。

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Corrigendum to “Centella asiatica as a potential neurotherapeutic adjunct in oxidative stress–targeted stem cell therapies” [Curr Opin Physiol, 46(2025) 1–7/100865] “积雪草作为氧化应激靶向干细胞治疗的潜在神经治疗辅助药物”的更正[j] .现代医学杂志，46(2025):1-7/100865。

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-11-19 DOI: 10.1016/j.cophys.2025.100873

Nuraliah F Mohd Fadzli, Siti SM Al Bakri, Norshariza Nordin

引用次数: 0

Targeting oxidative stress to combat neurodegenerative diseases, amyotrophic lateral sclerosis and Huntington’s, for better brain health and recovery 针对氧化应激对抗神经退行性疾病，肌萎缩性侧索硬化症和亨廷顿舞蹈症，促进大脑健康和恢复

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-10-30 DOI: 10.1016/j.cophys.2025.100872

Sofia Tanveer, Akarsh Bajpai, Shweta Jitendra Rajput, Preethi Saravanan, Basant K Patel

Amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD) are among neurodegenerative disorders (NDs) that are progressive, irreversible, debilitating and eventually lethal. Misfolding, aggregation and deposition of proteins such as mutant superoxide dismutase type-1 (SOD1), transactive response DNA-binding protein 43 (TDP-43) and fused in sarcoma (FUS) in ALS, and mutant huntingtin with polyglutamine expansion in HD, are implicated. Elevated level of reactive oxygen species, causing oxidative stress, is a pathological commonality among several NDs, including ALS and HD, which drives the damage to neuronal cell physiology and homeostasis. In view of its high potential as a therapeutic target, here, we review the role of oxidative stress in the pathogenesis of ALS and HD and the currently pursued therapies targeting oxidative stress, including the FDA-approved drugs and other novel therapeutic strategies presently under investigation.

肌萎缩性侧索硬化症（ALS）和亨廷顿氏病（HD）属于神经退行性疾病（NDs），它们是进行性、不可逆、使人衰弱并最终致命的。蛋白质的错误折叠，聚集和沉积，如突变型超氧化物歧化酶1 (SOD1)，交换性反应dna结合蛋白43 （TDP-43）和融合在肉瘤（FUS）中，以及突变型亨廷顿蛋白与聚谷氨酰胺扩增在HD中，涉及。活性氧水平升高，引起氧化应激，是包括ALS和HD在内的几种NDs的病理共性，它会导致神经元细胞生理和体内平衡的损害。鉴于其作为治疗靶点的巨大潜力，本文综述了氧化应激在ALS和HD发病机制中的作用，以及目前针对氧化应激的治疗方法，包括fda批准的药物和其他正在研究的新治疗策略。

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Visceral adipose tissue and the female heart: mechanisms and implications 内脏脂肪组织和女性心脏：机制和意义

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-10-24 DOI: 10.1016/j.cophys.2025.100871

Muhammad A Fahim , Yao Yao , Wanling Xuan

Heart failure with preserved ejection fraction (HFpEF) is an increasingly prevalent clinical challenge, particularly among aging and postmenopausal women. Emerging evidence highlights a significant role of adipose tissue, especially adipose tissue surrounding the heart, in the pathogenesis of HFpEF. Visceral fat depots function as endocrine and inflammatory organs. Coupled with hormonal changes during menopause, adipose tissue contributes to cellular senescence and myocardial dysfunction. This brief review summarizes the mechanistic links among adipose tissue, sex hormones, and depot-specific inflammation in HFpEF, and underscores potential targets for future research and therapeutic intervention.

心力衰竭伴射血分数保留（HFpEF）是一个日益普遍的临床挑战，特别是在老年和绝经后妇女中。新出现的证据强调了脂肪组织，特别是心脏周围的脂肪组织在HFpEF发病机制中的重要作用。内脏脂肪库具有内分泌和炎症器官的功能。再加上更年期荷尔蒙的变化，脂肪组织会导致细胞衰老和心肌功能障碍。本文简要综述了HFpEF中脂肪组织、性激素和仓库特异性炎症之间的机制联系，并强调了未来研究和治疗干预的潜在目标。

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Pregnancy complications and later-life maternal cardiovascular health: mechanistic insights from animal models 妊娠并发症和晚年产妇心血管健康：来自动物模型的机制见解

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-10-16 DOI: 10.1016/j.cophys.2025.100870

Amanda A de Oliveira , Floor Spaans , Murilo E Graton , Christy-Lynn M Cooke , Sandra T Davidge

Cardiovascular disease (CVD) is the leading cause of death globally in both men and women. Sex differences exist in the onset, progression, and outcomes of CVD, with sex-specific factors such as pregnancy-related conditions likely contributing to these disparities. Preeclampsia (PE) and gestational diabetes mellitus (GDM) are two of the most common medical complications of pregnancy, affecting approximately 3–5% and 5–18%, respectively. Women with a history of PE or GDM are at a higher risk of developing CVD later in life. Still, the underlying mechanisms are not fully understood. This review presents an overview of the mechanisms underlying the development of PE and GDM, and discusses pathophysiological pathways revealed through animal models that could contribute to long-term maternal cardiovascular dysfunction.

心血管疾病（CVD）是全球男女死亡的主要原因。CVD的发病、进展和结局存在性别差异，性别特异性因素（如妊娠相关疾病）可能导致这些差异。子痫前期（PE）和妊娠期糖尿病（GDM）是两种最常见的妊娠并发症，分别影响约3-5%和5-18%。有PE或GDM病史的女性在以后的生活中患心血管疾病的风险更高。然而，潜在的机制还没有完全被理解。本文综述了PE和GDM发展的机制，并讨论了通过动物模型揭示的可能导致母体长期心血管功能障碍的病理生理途径。

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Centella asiatica as a potential neurotherapeutic adjunct in oxidative stress–targeted stem cell therapies 积雪草作为氧化应激靶向干细胞治疗的潜在神经治疗辅助物

IF 1.9 Q2 PHYSIOLOGY

Current Opinion in Physiology

Pub Date : 2025-10-10 DOI: 10.1016/j.cophys.2025.100865

Nuraliah Faiqah Mohd Fadzli , Siti Sarah Mustaffa Al Bakri , Norshariza Nordin

Neurodegenerative disorders are marked by the progressive deterioration of neurons in the central nervous system, often driven by oxidative stress (OS), which disrupts cellular redox balance, damages neural tissue, and fuels chronic neuroinflammation. Despite ongoing active research on possible treatments, there is still no known cure for these diseases, necessitating innovative therapeutic approaches, including the use of herbal extracts. This review explores the potential of Centella asiatica, a traditional medicinal plant rich in antioxidant compounds, as a neuroenhancer in neurotherapeutic strategies targeting OS. By scrutinising the intricate interplay of Centella asiatica’s phytochemical constituents, this review aims to give insights into how this natural extract could offer innovative therapeutic strategies for addressing the complexities and effective treatment modalities of neurodegenerative diseases, potentially via stem cell–based cellular and acellular therapies.

神经退行性疾病以中枢神经系统神经元的进行性退化为特征，通常由氧化应激（OS）驱动，氧化应激会破坏细胞氧化还原平衡，损害神经组织，并引发慢性神经炎症。尽管目前正在积极研究可能的治疗方法，但这些疾病仍然没有已知的治愈方法，因此需要采用创新的治疗方法，包括使用草药提取物。本文综述了积雪草（Centella asiatica）作为一种富含抗氧化化合物的传统药用植物，在针对OS的神经治疗策略中作为神经增强剂的潜力。通过仔细研究积雪草植物化学成分的复杂相互作用，本综述旨在深入了解这种天然提取物如何为解决神经退行性疾病的复杂性和有效治疗方式提供创新的治疗策略，可能通过干细胞为基础的细胞和非细胞治疗。

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