期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 134, 期 -, 页码 154-164出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2019.07.009
关键词
Small ubiquitin-related modifier; Myocardial ischemia/reperfusion injury; Key proteins
资金
- National Natural Science Foundation of China [81570326]
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 Ca2+ 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.
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