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揭示阻塞性睡眠呼吸暂停低通气综合征与血管衰老之间的分子和细胞联系。

Unveiling the molecular and cellular links between obstructive sleep apnea-hypopnea syndrome and vascular aging.

作者信息

Liu Wei, Zhang Le, Liao Wenhui, Liu Huiguo, Liang Wukaiyang, Yan Jinhua, Huang Yi, Jiang Tao, Wang Qian, Zhang Cuntai

机构信息

Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, Hubei 430030, China.

Key Laboratory of Vascular Aging, Ministry of Education, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, Hubei 430030, China.

出版信息

Chin Med J (Engl). 2025 Jan 20;138(2):155-171. doi: 10.1097/CM9.0000000000003352. Epub 2024 Dec 6.

DOI:10.1097/CM9.0000000000003352
PMID:39647991
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11745861/
Abstract

Vascular aging (VA) is a common etiology of various chronic diseases and represents a major public health concern. Intermittent hypoxia (IH) associated with obstructive sleep apnea-hypopnea syndrome (OSAHS) is a primary pathological and physiological driver of OSAHS-induced systemic complications. A substantial proportion of OSAHS patients, estimated to be between 40% and 80%, have comorbidities such as hypertension, heart failure, coronary artery disease, pulmonary hypertension, atrial fibrillation, aneurysm, and stroke, all of which are closely associated with VA. This review examines the molecular and cellular features common to both OSAHS and VA, highlighting decreased melatonin secretion, impaired autophagy, increased apoptosis, increased inflammation and pyroptosis, increased oxidative stress, accelerated telomere shortening, accelerated stem cell depletion, metabolic disorders, imbalanced protein homeostasis, epigenetic alterations, and dysregulated neurohormonal signaling. The accumulation and combination of these features may underlie the pathophysiological link between OSAHS and VA, but the exact mechanisms by which OSAHS affects VA may require further investigation. Taken together, these findings suggest that OSAHS may serve as a novel risk factor for VA and related vascular disorders, and that targeting these features may offer therapeutic potential to mitigate the vascular risks associated with OSAHS.

摘要

血管衰老(VA)是多种慢性疾病的常见病因,也是一个主要的公共卫生问题。与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)相关的间歇性缺氧(IH)是OSAHS诱发全身并发症的主要病理生理驱动因素。据估计,相当一部分OSAHS患者(40%至80%)患有合并症,如高血压、心力衰竭、冠状动脉疾病、肺动脉高压、心房颤动、动脉瘤和中风,所有这些都与血管衰老密切相关。本综述探讨了OSAHS和血管衰老共有的分子和细胞特征,重点介绍了褪黑素分泌减少、自噬受损、细胞凋亡增加、炎症和细胞焦亡增加、氧化应激增加、端粒缩短加速、干细胞耗竭加速、代谢紊乱、蛋白质稳态失衡、表观遗传改变以及神经激素信号失调。这些特征的积累和组合可能是OSAHS与血管衰老之间病理生理联系的基础,但OSAHS影响血管衰老的确切机制可能需要进一步研究。综上所述,这些发现表明OSAHS可能是血管衰老和相关血管疾病的一个新的危险因素,针对这些特征可能提供治疗潜力,以减轻与OSAHS相关的血管风险。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e61a/11745861/c42d4989c4bb/cm9-138-155-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e61a/11745861/a101a0f3d3c9/cm9-138-155-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e61a/11745861/c42d4989c4bb/cm9-138-155-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e61a/11745861/a101a0f3d3c9/cm9-138-155-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e61a/11745861/7b8f7fc2bfda/cm9-138-155-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e61a/11745861/3997bd9c1098/cm9-138-155-g003.jpg
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