Adipokines in atherosclerosis: unraveling complex roles

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, adiponecti...

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Published inFrontiers in cardiovascular medicine Vol. 10; p. 1235953
Main Authors Luo, Jiaying, He, Zhiwei, Li, Qingwen, Lv, Mengna, Cai, Yuli, Ke, Wei, Niu, Xuan, Zhang, Zhaohui
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 14.08.2023
Subjects
adipokine
atherosclerosis
Cardiovascular Medicine
endothelial cell
macrophage
vascular smooth muscle cell
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Summary: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.
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These authors have contributed equally to this work and share first authorship
Reviewed by: Di Wang, Shanghai Jiao Tong University School of Medicine, China Chongxiu Sun, Nanjing Medical University, China Ibrahim AlZaim, Aarhus University, Denmark Zhaohua Cai, Shanghai Jiao Tong University, China Sathish Babu Vasamsetti, University of Pittsburgh, United States
Edited by: Adriana Georgescu, Institute of Cellular Biology and Pathology (ICBP), Romania
ISSN:2297-055X
2297-055X
DOI:10.3389/fcvm.2023.1235953