Adipokines in atherosclerosis: unraveling complex roles

Frontiers in Cardiovascular Medicine

Cardiovascular Medicine

Qingwen Li¹  Yuli Cai²  Mengna Lv³  Zhaohui Zhang³  Zhiwei He³  Xuan Niu³  Jiaying Luo³  Wei Ke³ 

[1]Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China

[2]Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, China

[3]Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, China

关键词: adipokine;    atherosclerosis;    endothelial cell;    vascular smooth muscle cell;    macrophage;   

DOI  :  10.3389/fcvm.2023.1235953

 received in 2023-06-07, accepted in 2023-08-02,  发布年份 2023

来源: Frontiers

【 摘 要 】

Adipokines are biologically active factors secreted by adipose tissue that act on local and distant tissues through autocrine, paracrine, and endocrine mechanisms. However, adipokines are believed to be involved in an increased risk of atherosclerosis. Classical adipokines include leptin, adiponectin, and ceramide, while newly identified adipokines include visceral adipose tissue-derived serpin, omentin, and asprosin. New evidence suggests that adipokines can play an essential role in atherosclerosis progression and regression. Here, we summarize the complex roles of various adipokines in atherosclerosis lesions. Representative protective adipokines include adiponectin and neuregulin 4; deteriorating adipokines include leptin, resistin, thrombospondin-1, and C1q/tumor necrosis factor-related protein 5; and adipokines with dual protective and deteriorating effects include C1q/tumor necrosis factor-related protein 1 and C1q/tumor necrosis factor-related protein 3; and adipose tissue-derived bioactive materials include sphingosine-1-phosphate, ceramide, and adipose tissue-derived exosomes. However, the role of a newly discovered adipokine, asprosin, in atherosclerosis remains unclear. This article reviews progress in the research on the effects of adipokines in atherosclerosis and how they may be regulated to halt its progression.

【 授权许可】

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© 2023 Luo, He, Li, Lv, Cai, Ke, Niu and Zhang.