Roles and mechanisms of SUMOylation on key proteins in myocardial ischemia/reperfusion injury.

Myocardial ischemia/reperfusion (MI/R) injury has a great influence on the prognosis of patients with acute coronary occlusion. The underlying mechanisms of MI/R injury are complex. While the incidence of MI/R injury is increasing every year, the existing therapies are not satisfactory. Recently, small ubiquitin-related modifier (SUMO), which is a post-translational modification and involved in many cell processes, was found to play remarkable roles in MI/R injury. Several proteins that can be SUMOylated were found to interfere with different mechanisms of MI/R injury. Sarcoplasmic reticulum Ca ATPase pump SUMOylation alleviated calcium overload. Among the histone deacetylase (HDAC) members, SUMOylation of HDAC4 reduced reactive oxygen species generation, whereas Sirt1 played protective roles in the SUMOylated form. Dynamic-related protein 1 modified by different SUMO proteins exerted opposite effects on the function of mitochondria. SUMOylation of hypoxia-inducible factors was fundamental in oxygen homeostasis, while eukaryotic elongation factor 2 SUMOylation induced cardiomyocyte apoptosis. The impact of other SUMOylation substrates in MI/R injury remains unclear. Here we reviewed how these SUMOylated proteins alleviated or exacerbated myocardial impairments by effecting the MI/R injury mechanisms. This may suggest methods for relieving MI/R injury in clinical practice and provide a reference for further study of SUMOylation in MI/R injury.