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极端温度暴露导致的慢性阻塞性肺疾病风险:将流行病学证据与病理生理机制相结合

COPD risk due to extreme temperature exposure: combining epidemiological evidence with pathophysiological mechanisms.

作者信息

Xu Jiayu, Xu Guogang, Liu Zehua, Hou Ruoyu, Ji John S, Huang Cunrui

机构信息

Vanke School of Public Health, Tsinghua University, Beijing, China.

Health Management Institute, The Second Medical Center & National Clinical Research Center for Geriatric Diseases, Chinese PLA General Hospital, Beijing, China.

出版信息

EBioMedicine. 2025 Apr 30;116:105731. doi: 10.1016/j.ebiom.2025.105731.

Abstract

Climate change is amplifying the frequency and intensity of extreme temperature events, posing a significant risk for chronic obstructive pulmonary disease (COPD). This review synthesised epidemiological evidence linking extreme temperature to COPD morbidity and mortality, while elucidating synergistic interactions with other environmental exposures. Combining population-level findings with biomedical mechanistic insights, we proposed a framework illustrating how biomarkers bridge the gap between extreme temperature exposure and COPD, highlighting the pathophysiological mechanisms of prodromal symptoms, key pathogenic processes and early molecular events. The mechanisms and biomarkers identified in this study would provide critical information for elucidating the causal pathways through which extreme temperatures increase COPD risk, and thus inform preventive interventions. Future research should incorporate multi-omics techniques to explore the underlying mechanisms in greater depth, while validating the biomarkers through large-scale cohort studies.

摘要

气候变化正在加剧极端温度事件的频率和强度,给慢性阻塞性肺疾病(COPD)带来重大风险。本综述综合了将极端温度与COPD发病率和死亡率联系起来的流行病学证据,同时阐明了与其他环境暴露的协同相互作用。结合人群水平的研究结果与生物医学机制见解,我们提出了一个框架,说明生物标志物如何弥合极端温度暴露与COPD之间的差距,突出前驱症状的病理生理机制、关键致病过程和早期分子事件。本研究中确定的机制和生物标志物将为阐明极端温度增加COPD风险的因果途径提供关键信息,从而为预防干预提供依据。未来的研究应采用多组学技术更深入地探索潜在机制,同时通过大规模队列研究验证生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a85c/12088773/3026f50fb55f/gr1.jpg

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