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Updated: Mar 22, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
HDAC9 regulates ox-LDL-induced endothelial cell apoptosis by participating in inflammatory reactions
Xu Han1, Xiang Han1, Zheng Wang1
1Department of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology of Fudan University, Shanghai, 200040, China.
Abstract:
Atherosclerosis is the most common cause of cardiovascular diseases worldwide. The endothelial cell apoptosis elicited by oxidized low-density lipoprotein (ox-LDL), which contributes to endothelial damage and inflammation, is a particularly important event in the early stage of atherosclerosis. However, the mechanism underlying ox-LDL-induced endothelial cell apoptosis remains unclear. Here we found that HDAC9 expression was increased at both the mRNA and protein levels accompanied by dose-dependent ox-LDL-induced endothelial cell apoptosis. Depletion of HDAC9 by its specific shRNA significantly antagonized ox-LDL-induced cell apoptosis and suppressed the expression of ox-LDL-induced inflammatory factors, such as TNF-alpha and MCP1. These data suggest that HDAC9 is an important epigenetic factor regulating ox-LDL-induced endothelial cell apoptosis and inflammatory factor expression. These results suggest that HDAC9 may participate in ox-LDL-induced endothelial damage and inflammation during atherosclerosis development.
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