LKB1 Regulates Vascular Macrophage Functions in Atherosclerosis

Frontiers in Pharmacology

Hong Xiang¹  Hongwei Lu¹  Shuhua Chen²  Xuewen Wang³  Ziwei Liang⁴  Yanqiu Li⁵ 

[1] Center for Experimental Medicine, The Third Xiangya Hospital of Central South University, Changsha, China;Department of Biochemistry, School of Life Sciences of Central South University, Changsha, China;Department of Cardiology, The Third Xiangya Hospital of Central South University, Changsha, China;Department of Clinical Laboratory, Yueyang people’s Hospital, Yueyang, China;Health Management Center, The Third Xiangya Hospital of Central South University, Changsha, China;

关键词: liver kinase B1;    atherosclerosis;    macrophage function;    AMPK;    inflammatory;   

DOI  :  10.3389/fphar.2021.810224

来源: DOAJ

【 摘 要 】

Liver kinase B1 (LKB1) is known to shape the regulation of macrophage function by participating in multiple processes including cell metabolism, growth, and polarization. However, whether LKB1 also affects the functional plasticity of macrophages in atherosclerosis has not attracted much attention. Abnormal macrophage function is a pathophysiological hallmark of atherosclerosis, characterized by the formation of foam cells and the maintenance of vascular inflammation. Mounting evidence supports that LKB1 plays a vital role in the regulation of macrophage function in atherosclerosis, including affecting lipid metabolism reprogramming, inflammation, endoplasmic reticulum stress, and autophagy in macrophages. Thus, decreased expression of LKB1 in atherosclerosis aggravates vascular injury by inducing excessive lipid deposition in macrophages and the formation of foam cells. To systematically understand the role and potential mechanism of LKB1 in regulating macrophage functions in atherosclerosis, this review summarizes the relevant data in this regard, hoping to provide new ideas for the prevention and treatment of atherosclerosis.

【 授权许可】

Unknown