期刊
FRONTIERS IN CARDIOVASCULAR MEDICINE
卷 8, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcvm.2021.663832
关键词
miR-135b-3p; ferroptosis; GPX4; cardiomyocyte ferroptosis; myocardial ischemia/reperfusion injury & nbsp;
资金
- Natural Science Foundation of Jiangsu, China [BK20201500]
- Jiangsu Province Traditional Chinese Medicine Leading Talent Project [SLJ0204]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (Integration of Chinese and Western Medicine)
- 333 High-level Talent Training Project of Jiangsu Province [BRA2020386]
The study found that miR-135b-3p promotes ferroptosis in cardiomyocyte ischemia/reperfusion injury by inhibiting the GPX4 gene. This provides a new therapeutic target for improving I/R injury.
Ferroptosis is a form of cell death induced by excess iron and accumulation of reactive oxygen species in cells. Recently, ferroptosis has been reported to be associated with cancer and ischemia/reperfusion (I/R) injury in multiple organs. However, the regulatory effects and underlying mechanisms of myocardial I/R injury are not well-understood. The role of miR-135b-3p as an oncogene that accelerates tumor development has been confirmed; however, its role in myocardial I/R is not fully understood. In this study, we established an in vivo myocardial I/R rat model and an in vitro hypoxia/reoxygenation (H/R)-induced H9C2 cardiomyocyte injury model and observed that ferroptosis occurred in tissues and cells during I/R myocardial injury. We used database analysis to find miR-135b-3p and validated its inhibitory effect on the ferroptosis-related gene glutathione peroxidase 4 (Gpx4), using a luciferase reporter assay. Furthermore, miR-135b-3p was found to promote the myocardial I/R injury by downregulating GPX4 expression. The results of this study elucidate a novel function of miR-135b-3p in exacerbating cardiomyocyte ferroptosis, providing a new therapeutic target for improving I/R injury.
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