The aim of this study was to investigate the protective effect of Cyclovirobuxine D (CVB-D) in myocardial infarction model and its potential molecular mechanism. By establishing an animal model of myocardial infarction and a cell model induced by hypoxia in vitro, we observed that CVB-D can alleviate tissue damage after myocardial infarction, improve cardiac function, and reduce cardiac fibrosis. At the cellular level, CVB-D enhanced autophagy and patted autophagy flow in cardiomyocytes after hypoxia, which was manifested as an increase in the ratio of autophagy related protein LC3-II/I, an increase in Lamp1 expression and a decrease in p62 expression. Further molecular mechanism studies suggest that CVB-D may promote autophagy of cardiomyocytes by activating Ets1/Mcl-1 signaling pathway and alleviate myocardial cell damage caused by hypoxia. These findings provide new strategies and potential drug targets for the treatment of myocardial infarction, as well as new insights into the mechanism of autophagy regulation in cardiomyocytes under stress. Future studies will continue to explore the potential application of CVB-D in the treatment of cardiovascular disease and further elucidate its molecular mechanism of action.

Nuo Chen, Yu Han, Rongzhou Wu. The mechanism of Ets1/Mgl-1 pathway impairment of circovirus B protein D. Frontiers in Medical Science Research (2024), Vol. 6, Issue 12: 72-82. https://doi.org/10.25236/FMSR.2024.061211.

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