The role of autophagy in pulmonary hypertension: a double-edge sword

被引：36
作者：
Chen, Rui [1 ]
Jiang, Meiping [1 ]
Li, Bo [1 ]
Zhong, Wei [1 ]
Wang, Zhongqun [1 ]
Yuan, Wei [1 ]
Yan, Jinchuan [1 ]
机构：
[1] Jiangsu Univ, Affiliated Hosp, Dept Cardiol, Zhenjiang 212001, Jiangsu, Peoples R China
来源：
APOPTOSIS | 2018年 / 23卷 / 9-10期
基金：
中国国家自然科学基金;
关键词：
Pulmonary hypertension; Autophagy; Pulmonary vascular remodeling; Right ventricular myocyte; HYPOXIA-INDUCED AUTOPHAGY; NITRIC-OXIDE SYNTHASE; ARTERIAL-HYPERTENSION; ENDOTHELIAL-CELLS; MOLECULAR-MECHANISMS; MAMMALIAN TARGET; OXIDATIVE STRESS; HUMAN-DISEASE; II RECEPTOR; BECLIN;
D O I：
10.1007/s10495-018-1477-4
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Autophagy is a recycling process that degrades damaged or unneeded cellular components for renewal. Accumulating evidence suggests that dysregulation of autophagy is involved in pulmonary hypertension (PH). PH is a progressive disease characterized by persistent proliferation of apoptosis-resistant pulmonary vascular cells. However, reports on the role of autophagy in the development of PH are often conflicting. In this review, we discuss recent development in the field with emphasis on pulmonary arterial endothelial cells, pulmonary smooth muscle cells, right ventricular myocyte, as well as pharmacological strategies targeting the autophagic signaling pathway.
引用
收藏
页码：459 / 469
页数：11
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