C1q/TNF-related protein 1: a novel link between visceral fat and athero-inflammation

This editorial refers to ‘C1q/tumour necrosis factor-related protein 1: an adipokine marking and promoting atherosclerosis’, by L. Lu et al ., doi:10.1093/eurheartj/ehv649. Approximately 30% of the global population are overweight or obese, posing a major threat to healthcare in developed and developing countries. Obesity decreases life expectancy, mainly by increasing the risk of type 2 diabetes and cardiovascular disease. A mechanistic explanation for these intertwined metabolic and cardiovascular risks has been offered by adipokines, a large and diverse group of molecules secreted by adipose tissue that affect both glucose metabolism and cardiovascular function. Importantly, the perivascular depot of adipose tissue is situated around the majority of the arterial tree, and a large number of studies have shown that local adipokine expression controls vascular function and dysfunction.1 Well-known adipokines include cytokines such as interleukin-1β and tumour necrosis factor α (TNFα) (resulting in the term adipose tissue-derived cytokines), leptin, and fatty acids. Among the most intriguing adipokines are the 16-member family of C1q/TNF-related proteins (CTRPs) that includes the intensively studied adiponectin,2 also synthesized in arterial perivascular adipose tissue (PVAT).3 The CTRPs share the globular adiponectin domain in their molecular structure, which binds and activates the adiponectin receptors AdipoR1 and AdipoR2, widely expressed in the cardiovascular system.4 CTRPs circulate as monomers but also as heterotrimers, enabling diverse biological effects.2 Figure 1 The adipokine CTRP1 (C1q/tumour necrosis factor-related protein 1) is produced in adipose tissue (yellow area) as well by oxidized LDL (OxLDL)- or interleukin-1β (IL-1β)-stimulated macrophages and endothelial cells in the atherosclerotic plaque (purple area). In the plaque, CTRP1 activates endothelial cells and macrophages themselves to produce leucocyte adhesion molecules and tumour necrosis factor α (TNFα), …