Histone modification of endothelial-mesenchymal transition in cardiovascular diseases

Abstract

Endothelial-mesenchymal transition (EndMT) is a differentiation process in which endothelial cells lose their own characteristics and acquire mesenchymal-like characteristics, which contributes to the formation and development of atherosclerotic plaques. Until now, there is still a lack of effective measures to treat atherosclerosis (AS), so there is an urgent need to understand the underlying mechanisms of AS. In addition, although various studies have shown that EndMT is involved in the pathological stages of cardiovascular diseases, such as myocardial fibrosis, myocardial hypertrophy, and hypertension, the specific molecular mechanisms driving EndMT are still in the exploratory stage. In this review, we review the role of histone modifications (methylation, demethylation and acetylation, deacetylation) on EndMT in cardiovascular disease, aiming to target histone-modifying enzymes to guide cardiovascular disease therapy.

Protective effect of rubber seed oil on human endothelial cells

“…It can act on endothelial cells to stimulate the secretion of chemokines such as MCP-1, IL-6 and IL-1β and up regulate the expression of adhesion molecules such as VCAM-1 on the cell surface (Kattoor et al 2019;Khosravi et al 2019;Jun et al 2022;Munjal and Khandia 2020;Ridker et al 2011;Lin et al 2014;Preiss and Sattar 2007). Subsequently, endothelial cell activation occurs from the oxidation reaction of these inflammatory mediators, leading to the expression of P-selectin (Woollard and Chin-Dusting 2007), E-selectin (Wenzel et al 1994), attracts the aggregation and adhesion of monocytes, and thus promote the progress of AS process.…”