Abstract
Purpose of ReviewIn 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 FindingsRecent 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.SummaryResearch 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.
Highlights
Endothelial dysfunction, inflammatory response, and metabolic dysregulation are key factors involved in initiation and progression of coronary artery disease (CAD) [1, 2]
Epicardial adipose tissue (EAT) is located inside the pericardial sac, which is adjacent to the epicardium surrounding the heart
EAT is considered a metabolically active organ with endocrine activity. It can secrete a large amount of inflammatory adipocytokines, of which, adiponectin is a well-known cardiovascular protective factor [3, 4]
Summary
Endothelial dysfunction, inflammatory response, and metabolic dysregulation are key factors involved in initiation and progression of coronary artery disease (CAD) [1, 2]. Epicardial adipose tissue (EAT) is located inside the pericardial sac, which is adjacent to the epicardium surrounding the heart. EAT is considered a metabolically active organ with endocrine activity. It can secrete a large amount of inflammatory adipocytokines, of which, adiponectin is a well-known cardiovascular protective factor [3, 4]. The C1q complement/ tumor necrosis factor (TNF)–associated proteins (CTRPs) superfamily is a paralog of adiponectin, composed of CTRP1CTRP15, which share a common structural domain with adiponectin [5]. CTRPs mRNA showed highest expression in white adipose tissue around the heart, making it the main
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