The roles of microRNA-22 in myocardial infarction.
- Author:
Bin-Hai CONG
1
;
Xiao-Yan ZHU
1
;
Xin NI
2
Author Information
1. Department of Physiology, The Second Military Medical University, Shanghai 200433, China.
2. Department of Physiology, The Second Military Medical University, Shanghai 200433, China. nixin@smmu.edu.cn.
- Publication Type:Journal Article
- From:
Acta Physiologica Sinica
2017;69(5):571-578
- CountryChina
- Language:English
-
Abstract:
Myocardial infarction (MI) is the leading cause of morbidity and mortality worldwide. The regeneration capacity of the adult mammalian heart is very limited, so that the lost cells are replaced by fibrotic scar. This is followed by remodeling of the surrounding myocardium, which includes cardiac hypertrophy and fibrosis, and makes the ventricular wall thicken and stiffen. This adverse cardiac remodeling leads to impaired cardiac function and eventually leads to heart failure. Extensive studies have revealed that microRNAs (miRNAs) play an essential role in cardiovascular diseases. microRNA-22 (miR-22) is one of the most abundant miRNA in the heart. Many studies have demonstrated that miR-22 plays critical roles in MI and subsequent cardiac remodeling. In this review, we summarized the recent research progresses, including the regulatory effects of miR-22 in oxidative stress, cardiac apoptosis, autophagy, hypertrophy, fibrosis and regeneration.
