MAPK/ERK通路
生物
细胞生物学
心肌梗塞
胚胎干细胞
心功能曲线
调节器
细胞生长
胚胎心脏
心肌细胞
信号转导
癌症研究
内科学
心力衰竭
医学
遗传学
基因
作者
Ke Feng,Yukang Wu,Jianguo Li,Qiaoyi Sun,Zihui Ye,Xuan Li,Xudong Guo,Jiuhong Kang
出处
期刊:Stem Cells
[Oxford University Press]
日期:2023-11-02
卷期号:42 (1): 29-41
被引量:4
标识
DOI:10.1093/stmcls/sxad080
摘要
Abstract Poor proliferative capacity of adult cardiomyocytes is the primary cause of heart failure after myocardial infarction (MI), thus exploring the molecules and mechanisms that promote the proliferation of adult cardiomyocytes is crucially useful for cardiac repair after MI. Here, we found that miR-130b-5p was highly expressed in mouse embryonic and neonatal hearts and able to promote cardiomyocyte proliferation both in vitro and in vivo. Mechanistic studies revealed that miR-130b-5p mainly promoted the cardiomyocyte proliferation through the MAPK-ERK signaling pathway, and the dual-specific phosphatase 6 (Dusp6), a negative regulator of the MAPK-ERK signaling, was the direct target of miR-130b-5p. Moreover, we found that overexpression of miR-130b-5p could promote the proliferation of cardiomyocytes and improve cardiac function in mice after MI. These studies thus revealed the critical role of miR-130b-5p and its targeted MAPK-ERK signaling in the cardiomyocyte proliferation of adult hearts and proved that miR-130b-5p could be a potential target for cardiac repair after MI.
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