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AGEs-Induced Calcification and Apoptosis in Human Vascular Smooth Muscle Cells Is Reversed by Inhibition of Autophagy.

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机构： [1]Dr. Neher’s Biophysics Laboratory for Innovative Drug Discovery, State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China, [2]Department of Vascular Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, China, [3]Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Macau, China, [4]Department of Nuclear Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, China, [5]Nuclear Medicine and Molecular Imaging Key Laboratory of Sichuan Province, Luzhou, China, [6]Laboratory of Chinese Materia Medical, School of Pharmacy, Southwest Medical University, Luzhou, China, [7]Institute of Cardiovascular Research, The Key Laboratory of Medical Electrophysiology, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease of Sichuan Province, Southwest Medical University, Luzhou, China, [8]Affiliated Hospital of Ya’an Polytechnic College, Ya’an, China

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关键词： autophagy ATG7 ages HASMCs calcification apoptosis

摘要：

Vascular calcification (VC) in macrovascular and peripheral blood vessels is one of the main factors leading to diabetes mellitus (DM) and death. Apart from the induction of vascular calcification, advanced glycation end products (AGEs) have also been reported to modulate autophagy and apoptosis in DM. Autophagy plays a role in maintaining the stabilization of the external and internal microenvironment. This process is vital for regulating arteriosclerosis. However, the internal mechanisms of this pathogenic process are still unclear. Besides, the relationship among autophagy, apoptosis, and calcification in HASMCs upon AGEs exposure has not been reported in detail. In this study, we established a calcification model of SMC through the intervention of AGEs. It was found that the calcification was upregulated in AGEs treated HASMCs when autophagy and apoptosis were activated. In the country, AGEs-activated calcification and apoptosis were suppressed in Atg7 knockout cells or pretreated with wortmannin (WM), an autophagy inhibitor. These results provide new insights to conduct further investigations on the potential clinical applications for autophagy inhibitors in the treatment of diabetes-related vascular calcification.Copyright © 2021 He, Qu, Kwan Law, Qiu, Han, Ricardo de Seabra Rodrigues Dias, Liu, Zhang, Wu, Wu, Fai Mok, Cheng, He and Wai Wong.

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出版当年[2020]版：

大类 | 2 区医学

小类 | 2 区药学

最新[2025]版：

大类 | 3 区医学

小类 | 3 区药学

第一作者：

第一作者机构： [1]Dr. Neher’s Biophysics Laboratory for Innovative Drug Discovery, State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China, [2]Department of Vascular Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, China,

通讯作者：

通讯机构： [1]Dr. Neher’s Biophysics Laboratory for Innovative Drug Discovery, State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China, [3]Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, Macau, China,

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AGEs-Induced Calcification and Apoptosis in Human Vascular Smooth Muscle Cells Is Reversed by Inhibition of Autophagy.

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