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 F-box and WD repeat domain containing 7 (Fbw7) and MCL1 apoptosis regulator, BCL2 family member (Mcl-1) in myocardial cells during oxidative stress, Cell Counting Kit-8, flow cytometry, western blot, reactive oxygen species and co-immunoprecipitation assays were conducted. The current study revealed that Fbw7 may facilitate apoptosis via the Mcl-1-Bax pathway in oxidative stress-induced myocardial H9c2 cell injury. Mcl-1 inhibits the functions of Bcl-2 family members, including the mitochondrial apoptosis factor Bax, to maintain cell viability; however, the present study suggested that Fbw7 may degrade Mcl-1 and impaired this process. Therefore, it may be hypothesized that Fbw-7 promotes myocardial cell injury via interacting with Mcl-1.
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