C1q/tumor necrosis factor-related protein 13 (CTRP13) is a secreted adipokine that can ameliorate abnormal glucose and lipid metabolism. However, the functional role of CTRP13 in the development of atherosclerotic plaques has yet to be described. In this study, we collected blood samples from patients of coronary artery diseases and apolipoprotein E (ApoE)-/- mice that were fed a Western diet for 12 wk to induce atherosclerosis and found that serum CTRP13 level was decreased. En face staining of aortas and aortic sinus in ApoE-/- mice showed that ectopic CTRP13 infusion in vivo dramatically decreased lesion areas, as well as reduced inflammatory responses with less macrophage content. In primary peritoneal macrophages in vitro, CTRP13 supplement reduced oxidized LDL uptake, foam-cell formation, and trapping, together with the suppressed cluster of differentiation 36 (CD36) protein levels. Reduced CD36 protein level was attributed to the autophagy-lysosome-dependent degradation of CD36 at the post-transcriptional level. The blocking of autophagy-lysosome induction could increase CD36 protein level, foam-cell formation, and migration, thus abolishing the protective effects of CTRP13 on atherosclerosis. In summary, these findings define CTRP13 as a novel approach for preventing atherosclerotic plaque formation via modulation of lipid uptake and foam-cell migration.-Wang, C., Xu, W., Liang, M., Huang, D., Huang, K. CTRP13 inhibits atherosclerosis via autophagy-lysosome-dependent degradation of CD36.
Keywords: lipid uptake; macrophage; post-transcriptional; trapping.