The role of protein SUMOylation in the pathogenesis of atherosclerosis

Abstract

Atherosclerosis is a progressive, inflammatory cardiovascular disorder characterized by the development of lipid‐-filled plaques within arteries. Endothelial cell dysfunction in the walls of blood vessels results in an increase in vascular permeability, alteration of the components of the extracellular matrix, and retention of LDL in the sub‐-endothelial space, thereby accelerating plaque formation. Epigenetic modification by SUMOylation can influence the surface interactions of target proteins and affect cellular functionality, thereby regulating multiple cellular processes. Small ubiquitin‐-like modifier (SUMO) can modulate NFκB and other proteins such as p53, KLF, and ERK5, which have critical roles in atherogenesis. Furthermore, SUMO regulates leukocyte recruitment and cytokine release and the expression of adherence molecules. In this review, we discuss the regulation by SUMO and SUMOylation modifications of proteins and pathways involved in atherosclerosis.