Low Shear Stress Regulating Autophagy Mediated by the p38 Mitogen Activated Protein Kinase and p53 Pathways in Human Umbilical Vein Endothelial Cells

• Published in: Chinese medical journal Vol. 131; no. 9; pp. 1132 - 1133
• Main Authors: Liu, Hui-Zhen, Li, Li, Chen, Shao-Liang, Wei, Jian-Rui, Zhang, Jun-Xia, Liu, Jia, Guo, Jie-Wen, Qu, Xin-Liang, Chu, Peng
• Format: Journal Article
• Language: English
• Published: China Wolters Kluwer India Pvt. Ltd 05.05.2018; Medknow Publications and Media Pvt. Ltd; Lippincott Williams & Wilkins Ovid Technologies; Department of Cardiology, Guangzhou Red Cross Hospital, Jinan University affiliated Guangzhou Red Cross Hospital, Guangzhou, Guangdong 510000, China%Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China; Medknow Publications & Media Pvt Ltd; Wolters Kluwer
• Subjects: Autophagy; Cardiology; Cells, Cultured; Correspondence; Endothelium, Vascular - metabolism; Human Umbilical Vein Endothelial Cells - metabolism; Humans; Kinases; p38 Mitogen-Activated Protein Kinases - metabolism; Proteins; Shear stress; Stress, Mechanical; Tumor Suppressor Protein p53 - metabolism; @@
• ISSN: 0366-6999; 2542-5641
• DOI: 10.4103/0366-6999.230724

To the Editor: Autophagy is reported to play a critical role in low shear stress (LSS)-induced endothelial cell injury and the formation of atherosclerotic plaques. Light chain (LC) II, LC3 I, and p62, p38 mitogen-activated protein kinase (MAPK) and their protein of phosphorylation of p38 (p-p38) were detected with Western blot analysis. [...]this study concluded that LSS induced autophagy by activating the p38 MAPK signaling pathway and inhibited autophagy flux by the p53 pathway in HUVECs.