C1q/TNF-related protein-9 attenuates palmitic acid-induced endothelial cell senescence via increasing autophagy

Autophagy is an important process in the pathogenesis of atherosclerosis. C1q/tumor necrosis factor-related protein 9 (CTRP9) closest adiponectin paralog. CTRP9 has anti-aging and anti-atherogenic effects, but its roles autophagy endothelial senescence are currently unknown. This study aimed to evaluate whether prevents palmitic acid (PA)-induced by promoting autophagy. After no treatment or pre-treatment human umbilical vein cells with prior PA treatment, level was measured associated acidic ?-galactosidase staining hyperphosphorylated pRB protein. evaluated LC3 conversion p62/SQSTM1, a degraded during Autophagosome–lysosome fusion detected fluorescence microscopy. Pre-treatment attenuated PA-induced senescence. increased LC3-I LC3-II decreased p62 levels time- dose-dependent manner. Although both conversion, expression autophagosomes lysosomes, which represented autophagic flux. However, recovered flux inhibited PA. AMP-activated kinase (AMPK) activation involved induced CTRP9. inhibits recovering through AMPK activation.