Abstract
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.
Highlights
Atherosclerosis is a systemic vascular disease, which is the pathological basis of cardiovascular and cerebrovascular diseases such as coronary heart disease and stroke (Ibanez et al, 2021; Shea et al, 2021)
Liver kinase B1 (LKB1) is a serine-threonine kinase expressed in a variety of cells and is involved in regulating cell metabolism, polarity, and growth
LKB1’s regulation of macrophage lipid metabolism and its inhibition of foam cell formation are achieved by directly affecting the expression of scavenger receptors (SR) or indirectly regulating autophagy
Summary
Atherosclerosis is a systemic vascular disease, which is the pathological basis of cardiovascular and cerebrovascular diseases such as coronary heart disease and stroke (Ibanez et al, 2021; Shea et al, 2021). A substantial amount of low-density lipoprotein (LDL) is deposited in the arterial wall and is oxidized into oxidized LDL (Ox- LDL) This oxidized form of LDL cannot be recognized by the LDL receptors and internalized into cells for decomposition but is mainly recognized and taken up by macrophages through the scavenger receptors (SR) (Shen et al, 2020). As the main innate immune cells, macrophages play a key role in maintaining the inflammatory response of blood vessels and regulating the stability of atherosclerotic plaques by producing pro-inflammatory cytokines (Kim et al, 2021). Through AMPK, LKB1 regulates lipid metabolism, glycolysis, and other metabolic pathways to maintain the phenotype and function of normal cells (Zhang Y. et al, 2021; Molina et al, 2021). Given that the particular regulatory importance of LKB1 in macrophage function in atherosclerosis has not been systematically described, here we review the role and possible mechanism of LKB1 in shaping macrophage function to reveal the potential target for the treatment of atherosclerosis
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