E3连接酶Fbw7通过Mcl1-Bax通路参与氧化应激诱导的心肌细胞损伤

Abstract

Oxidative stress participates in several heart diseases and is an important mechanism contributing to the pathological alterations of myocardial cell injury. In recent years, ubiquitylation has been demonstrated to be an important biochemical reaction associated with apoptosis. To investigate the effects and interactions of the E3 ligase Fbox and WD repeat domain containing 7 (Fbw7) and MCL1 apoptosis regulator, BCL2 family member (Mcl1) in myocardial cells during oxidative stress, Cell Counting Kit8, flow cytometry, western blot, reactive oxygen species and coimmunoprecipitation assays were conducted. The current study revealed that Fbw7 may facilitate apoptosis via the Mcl1Bax pathway in oxidative stressinduced myocardial H9c2 cell injury. Mcl1 inhibits the functions of Bcl2 family members, including the mitochondrial apoptosis factor Bax, to maintain cell viability; however, the present study suggested that Fbw7 may degrade Mcl1 and impaired this process. Therefore, it may be hypothesized that Fbw7 promotes myocardial cell injury via interacting with Mcl1.