NR4A1 contributes to high-fat associated endothelial dysfunction by promoting CaMKII-Parkin-mitophagy pathways

• DOI: 10.1007/s12192-018-0886-1
• Publication Date: 2018-02-22T06:29:42Z
• Authors: Pei Li; Yuzhi Bai; Xia Zhao; Tian Tian; Liying Tang; Jing Ru; Yun An; Jing Wang
• Keywords: Endothelial Dysfunction

Parkin-related mitophagy is vital for endothelial cell viability and the development of atherosclerosis, although upstream regulatory factor underlying Parkin-mediated in apoptosis atherosclerosis progression remains unknown. In present study, we demonstrated that nuclear receptor subfamily 4 group A member 1 (NR4A1) actually expressed aortic cells (AECs) under oxidized low-density lipoprotein (ox-LDL) treatment vitro or isolated from high-fat treated mice vivo. Higher NR4A1 levels were associated with AEC apoptosis, mitochondrial dysfunction, energy disorder. At molecular level, ox-LDL stimulation increased expression, which evoked mitophagy. Excessive overtly consumed mass, leading to an shortage dysfunction. However, loss protected AECs against induced by inhibiting excessive Furthermore, also identified regulated Parkin activation via post-transcriptional modification Ca2+/calmodulin-dependent protein kinase II (CaMKII). Activated CaMKII phosphorylated Parkin. summary, our data support role NR4A1/CaMKII/Parkin/mitophagy formation provide new insights into treating respect viability, mitophagy, NR4A1.