Macrophage origin, phenotypic diversity, and modulatory signaling pathways in the atherosclerotic plaque microenvironment

Abstract

Atherosclerosis is the main pathological basis of most cardiovascular diseases and the

Acid external and internal environment exchange the Oreochromis niloticus tissue immune gene expression compared to the mouse macrophage polarization model

“…Further, G protein-coupled receptor 132 (Gpr132) has been shown to function as a key macrophage sensor of the rising lactate in the acidic milieu to mediate the reciprocal interaction between cancer cells and macrophages ( 44 ). One previous study showed that macrophage M2 marker, including arginase-1 ( Arg1 ), Mgl-1 , Kruppel-like factor 4 ( KLF4 ), and found in inflammatory zone 1 (Fizz1 ) ( 45 ). Furthermore, IL-10 has been shown to promote macrophage polarization.…”

Low-density lipoprotein particles in atherosclerosis

“…The higher the amount of LDL being trapped in the subendothelium, the faster the atherosclerotic plaque evolves ( Rosenson and Underberg, 2013 ; Liu et al, 2021b ; Lin et al, 2021 ). It is worth noting that only after modifications, such as oxidation and desialylation, LDL particles become atherogenic.…”

“…Growth factors mediate proliferation of smooth muscle cell and formation of extracellular matrix. Platelet adherence and accumulation are also, in part elicited by ox-LDL which result into a rupture prone thrombus ( Kruth et al, 2002 ; Yoshida, 2010 ; Khatana et al, 2020 ; Liu et al, 2021b ; Lin et al, 2021 ). The mechanisms of action of ox-LDL-induced atherosclerosis have been well-documented ( Matsuura et al, 2008 ; Khatana et al, 2020 ; Jiang et al, 2022 ).…”

Lipid-Laden Macrophages and Inflammation in Atherosclerosis and Cancer: An Integrative View

“…Notably, immunostained human coronary arteries showed that macrophages with similar antigen expression as induced in vitro by M-CSF, i.e., the M2-like macrophage phenotype, were predominant within human atherosclerotic lesions ( 69 ). Interestingly, the distribution of macrophage subtypes is not uniform in human atherosclerotic plaques, being M1 macrophages located at the rupture-prone shoulders of mature plaques while the M2 macrophages are away from the lipid core ( 70 ). Because GM-CSF and M-CSF are soluble glycoproteins widely expressed in the arterial intima ( 71 ) and the formation of cholesterol-loaded macrophage foam cells is intrinsically related to atherogenesis, we recently investigated the effect of cholesterol loading on the expression of key atheroinflammatory genes in cultured human monocyte-derived macrophages differentiated by either CSF ( 72 ).…”