期刊
RESPIRATORY RESEARCH
卷 22, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12931-021-01630-1
关键词
Chronic obstructive pulmonary disease; Cigarette smoke; Epigenetic; Gene regulation; Molecular biology; Apoptosis; Endothelial cell
资金
- National Natural Science Foundation of China [81970044]
COPD is a common chronic respiratory disease with smoking as a main risk factor. Recent research indicates that pulmonary vascular endothelial cell apoptosis plays a role in the pathogenesis of COPD.
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据