microRNA-22在心肌梗死中的作用（英文）

发布时间：2018-06-27 17:09

本文选题：microRNA + 心肌细胞　；参考：《生理学报》2017年05期

【摘要】：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。
[Abstract]:Myocardial infarction is a common clinical disease, because of its high incidence and mortality, has been highly concerned by the medical community. Myocardial infarction leads to cardiac myocyte death. As adult cardiomyocytes almost lose their regenerative ability, the repair of the injured heart is mainly achieved through fibrosis. At the same time, viable cardiomyocytes develop progressive hypertrophy to maintain the pumping function of the heart. However, fibrosis and hypertrophy also lead to cardiac remodeling, resulting in decompensation of heart function, and ultimately heart failure. Recent studies have shown that miRNA (miRNA) plays an important role in cardiovascular disease. MicroRNA-22 (miR-22) is a highly expressed miRNAs in the heart. Many studies have confirmed that miR-22 plays an important role in myocardial infarction and cardiac remodeling. In this paper, the main research progress in recent years is summarized, including the regulatory effects of miR-22 on oxidative stress, apoptosis, autophagy, myocardial hypertrophy, cardiac fibrosis and cardiac regeneration.
【作者单位】：第二军医大学生理学教研室;
【基金】：supported by grants from the Shanghai Science and Technology Committee (No. 16ZR1444300) the National Natural Science Foundation of China (No. 31671213)
【分类号】：R542.22

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