期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 461, 期 2, 页码 321-328出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2015.04.032
关键词
PDCD5; Autophagy; Cardiac remodeling
资金
- National Key Basic Research Program of China (973) [2011CB910103]
- National Natural Science Foundation of China [81272432, 81070260]
Cardiac remodeling, including cardiac hypertrophy and fibrosis, is an important pathological process that can lead to heart failure. A previous study demonstrated that autophagy could represent an active adaptive response in cardiomyocytes that affords protection from cardiac remodeling. In the present study, we investigated the role of an autophagy-related gene, PDCD5 (Programmed cell death 5), in cardiac remodeling induced by beta-adrenergic stimulation in vivo. We report for the first time that mice systemically overexpressing PDCD5 (PDCD5tg) were protected from cardiac remodeling. In addition, cardiac function was preserved in PDCD5tg mice in response to isoproterenol (ISO) stimulation. Importantly, basal autophagy was significantly higher in PDCD5tg mice than in the wild-type (WT) mice. Moreover, apoptosis was significantly lower in PDCD5tg mice than in WT mice, among the ISO-induced animals. In summary, our findings reveal that PDCD5 overexpression improves cardiac function and inhibits cardiac remodeling induced by ISO via induction of autophagy and inhibition of apoptosis. (C) 2015 Elsevier Inc. All rights reserved.
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