microRNA-22在心肌梗死中的作用（英文）

The roles of microRNA-22 in myocardial infarction

心肌梗死是临床常见的疾病,由于其极高的发病率和致死率,一直受到医学界的高度关注。心肌梗死导致心肌细胞死亡,由于成年心肌细胞几乎丧失再生能力,损伤后心脏的修复主要通过纤维化实现。同时,存活的心肌细胞进行性发生肥大,以维持心脏的泵血功能。然而,纤维化和肥大也导致了心脏重构,使心脏功能失代偿,最终发展为心力衰竭。近年来研究显示,microRNA(miRNA)在心血管疾病中具有重要的作用。microRNA-22(miR-22)作为一种在心脏中高表达的miRNA,许多研究已证实miR-22在心肌梗死及心脏重构的过程中发挥了重要作用。本文主要总结了近年来的主要研究进展,包括miR-22对氧化应激、细胞凋亡、细胞自噬、心肌肥大、心脏纤维化和心脏再生的调节作用。

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.