Post-Translational Modification of Drp1 is a Promising Target for Treating Cardiovascular Diseases

Mitochondria are essential for cell growth, fission, differentiation, and survival, particularly in undivided cells with high energy requirements, such as cardiomyocytes. The morphology and position of mitochondria change with the activity of mitochondrial fission proteins and mitochondrial fusion proteins. These regulatory mechanisms substantially affect cardiomyocyte energy supply and normal function. In mitochondrial fission, dynamin-related protein 1 (Drp1) is involved in the separation and degradation of damaged mitochondria, and accurately regulates mitochondrial renewal and number. Recent studies have revealed a variety of post-translational modification (PTMs) of Drp1, including phosphorylation, SUMOylation, acetylation, O-GlcNAcylation, and S-sulfhydration. These modifications ensure that Drp1 continues to function normally in various signaling pathways, by modulating its activity, stability, and subcellular localization. This article provides an overview of the relationship between Drp1 PTMs and cardiovascular diseases such as heart failure, myocardial infarction, and myocardial ischemia-reperfusion, and describes how these modifications can be targeted and regulated, to help guide cardiovascular disease treatment.