The role of cigarette smoke-induced pulmonary vascular endothelial cell apoptosis in COPD.

The role of cigarette smoke-induced pulmonary vascular endothelial cell apoptosis in COPD.
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香烟烟雾诱导肺血管内皮细胞凋亡在慢性阻塞性肺疾病中的作用

DOI:
10.1186/s12931-021-01630-1
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发表时间:
2021-02-05
影响因子:
5.8
通讯作者:
Liu XM
Liu XM
中科院分区:
医学2区
文献类型:
--
作者:
Song Q;Chen P;Liu XM

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慢性阻塞性肺疾病(COPD)是最常见的慢性呼吸道疾病之一,发病率和死亡率都很高。它已成为全球经济中第五大负担最重和第三大致命疾病,并逐年增加。预防和治疗慢性阻塞性肺病迫在眉睫。吸烟是慢性阻塞性肺病的主要和最常见的危险因素。香烟烟雾(CS)中含有大量有毒物质,可引起气管、肺组织、肺血管的一系列变化,促进COPD的发生和发展。近年来,表观遗传学和分子生物学的发展为揭示疾病的发病机制、诊断和治疗提供了新的指导。最新研究表明,肺血管内皮细胞凋亡启动并参与了COPD的发病过程。本文就cs诱导COPD肺血管内皮细胞凋亡的表观遗传机制和分子生物学研究现状进行综述,为COPD发病机制的研究提供新的研究方向,为COPD的诊断、治疗和预防提供新的靶点。
Chronic obstructive pulmonary disease (COPD) is one of the most common chronic respiratory diseases with high morbidity and mortality. It has become the fifth most burdened and the third most deadly disease in the global economy and increases year by year. The prevention and treatment of COPD are urgent. Smoking is the main and most common risk factor for COPD. Cigarette smoke (CS) contains a large number of toxic substances, can cause a series of changes in the trachea, lung tissue, pulmonary blood vessels, and promotes the occurrence and development of COPD. In recent years, the development of epigenetics and molecular biology have provided new guidance for revealing the pathogenesis, diagnosis, and treatment of diseases. The latest research indicates that pulmonary vascular endothelial cell apoptosis initiates and participates in the pathogenesis of COPD. In this review, we summarize the current research on the epigenetic mechanisms and molecular biology of CS-induced pulmonary vascular endothelial cell apoptosis in COPD, providing a new research direction for pathogenesis of COPD and a new target for the diagnosis, treatment, and prevention of COPD.
DOI: 10.1186/1465-9921-7-53
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