CTRP1 and CTRP5 act as pro-inflammatory risk factors for coronary artery disease, whereas CTRP3, CTRP9, CTRP12, and CTRP13 serve as protective factors by inhibiting inflammation and plaque formation.
PURPOSE OF REVIEW: In recent years, a family of adiponectin paralogs designated as C1q/TNF-related protein (CTRP) has attracted increasing attention. They are inflammatory adipocytokines mostly secreted from epicardial adipose tissue, which modulate the development and prognosis of coronary artery disease (CAD). This review summarizes the pathophysiological roles of individual members of the CTRP superfamily in the development of CAD. RECENT FINDINGS: Recent studies have revealed how members of the CTRP family, CTRP1, CTRP3, CTRP5, CTRP9, CTRP12, and CTRP13, can influence both development and progression of CAD by modulating metabolic pathways, influencing immuno-inflammatory response, and regulating cardiovascular functions. Research to date has not been sufficient to answer the specific mechanism of the CTRP family in the occurrence and development of CAD. This review explores the evidence of CTRP superfamily regulating different pathophysiology stages of CAD through the immuno-inflammation, glucose and lipid metabolism, and vascular endothelial function.
Si et al. (Thu,) conducted a review in Coronary artery disease. CTRP family proteins was evaluated. CTRP1 and CTRP5 act as pro-inflammatory risk factors for coronary artery disease, whereas CTRP3, CTRP9, CTRP12, and CTRP13 serve as protective factors by inhibiting inflammation and plaque formation.