The pathophysiological role of receptor-interacting protein kinase 3 in cardiovascular disease

Abstract

Recent studies have found that receptor interacting protein kinase 3 (RIPK3) can mediate CaMK Ⅱ phosphorylation and oxidation, open mitochondrial permeability transition pore (mPTP), and induce myocardial necroptosis. The increased expression or phosphorylation of RIPK3 is one of the important markers of necroptosis; Inhibition of CaMK Ⅱ phosphorylation or oxidation significantly reduces RIPK3 mediated myocardial necroptosis; Studies have shown that necroptosis plays an important role in the occurrence and development of cardiovascular diseases; Using the selective inhibitor GSK '872 of RIPK3 can effectively inhibit the occurrence and development of cardiovascular diseases, and can reverse cardiovascular and cardiac dysfunction caused by overexpression of RIPK3. In this review, we provide a brief overview of the current knowledge on RIPK3 in mediating necroptosis, inflammatory response, and oxidative stress, and discussed the role of RIPK3 in cardiovascular diseases such as atherosclerosis, myocardial ischaemia, myocardial infarction, and heart failure.

Keywords: Cardiovascular diseases; Inflammation; Myocardial hypertrophy; Necroptosis; Oxidative stress; Receptor interacting protein kinase 3 (RIPK3).