Xiao Xuan, Liu Yi-Zhang, Cheng Zhe-Bin, Sun Jia-Xiang, Shao Yi-Duo, Qu Shun-Lin, Huang Liang, Zhang Chi
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.
Clin Chim Acta. 2021 May;516:15-26. doi: 10.1016/j.cca.2021.01.009. Epub 2021 Jan 18.
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.
脂肪组织(AT)是一种重要的内分泌腺,能够产生和分泌大量的脂肪因子。脂肪因子通过旁分泌、自分泌和内分泌机制作用于远处或邻近的器官组织,在糖脂代谢和炎症反应的调节中发挥着重要作用。越来越多的证据表明,脂肪因子可作为血管钙化的促进剂或抑制剂,将肥胖与心血管疾病联系起来。由脂肪细胞肥大引起的AT慢性缺氧能够引发脂肪因子生成失衡,进而导致细胞凋亡、血管平滑肌细胞(VSMC)的成骨分化、血管炎症以及血管壁中钙和磷的异常沉积。本综述的目的是简要总结主要脂肪因子对血管钙化形成和发展的关键影响,这可能有助于更好地理解这些脂肪因子,从而制定适当的治疗策略来对抗肥胖相关的血管钙化。