Adipokines in vascular calcification.

Xuan Xiao, Yi-Zhang Liu, Zhe-Bin Cheng, Jia-Xiang Sun, Yi-Duo Shao, Shun-Lin Qu, Liang Huang, Chi Zhang

Journal: Clinica chimica acta; international journal of clinical chemistry 2021;516():15-26

PMID: 33476587

Abstract

Adipose tissue (AT), a critical endocrine gland, is capable of producing and secreting abundant adipokines. Adipokines act on distant or adjacent organ tissues via paracrine, autocrine, and endocrine mechanism, which play attractive roles in the regulation of glycolipid metabolism and inflammatory response. Increasing evidence shows that adipokines can connect obesity with cardiovascular diseases by serving as promoters or inhibitors in vascular calcification. The chronic hypoxia in AT, caused by the adipocyte hypertrophy, is able to trigger imbalanced adipokine generation, which leads to apoptosis, osteogenic differentiation of vascular smooth muscle cells (VSMCs), vascular inflammation, and abnormal deposition of calcium and phosphorus in the vessel wall. The objectives of this review aim at providing a brief summary of the crucial influence of major adipokines on the formation and development of vascular calcification, which may contribute to better understanding these adipokines for establishing the appropriate therapeutic strategies to counteract obesity-associated vascular calcification.

Copyright © 2021 Elsevier B.V. All rights reserved.

Address: Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China; Research Lab for Clinical & Translational Medicine, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China; Departments of Clinical Medicine, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China.; Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China; Research Lab for Clinical & Translational Medicine, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China; Departments of Stomatology, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China.; Departments of Clinical Medicine, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China.; Departments of Stomatology, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China.; Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China.; Research Lab for Clinical & Translational Medicine, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China. Electronic address: [email protected].; Institute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, Hengyang Medical College, University of South China, Hengyang, Hunan 421001, People's Republic of China. Electronic address: [email protected].

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