In both groups, CD36 MFI and mRNA were significantly higher in patients with diabetic atherosclerosis in comparison with those without diabetic atherosclerosis (P<0.05).
In conclusion, inhibition of CD36-mediated oxLDL uptake and induction of ABCA1- and ABCG1-dependent cholesterol efflux are two working mechanisms by which andrographolide inhibits macrophage foam cell formation, which suggests that andrographolide could be a potential candidate to prevent atherosclerosis.
In hematopoietic cells, CD36 signaling enhances platelet dysfunction thus decreasing the threshold for platelet activation and accelerating arterial thrombosis, whereas in macrophages, CD36 promotes lipid-laden foam cell formation and atherosclerosis.
In line with these in vitro observations, in the atherosclerosis-susceptible apolipoprotein E (ApoE) KO background, CPT2 M-KO mice demonstrated augmented atherosclerosis, accompanied by increased accumulation of aortic macrophages with elevated CD36 expression.
In this in vivo study, we investigated whether simvastatin downregulates the expression of CD36 and calpain-1 and inhibits the inflammation and atherosclerosis in apolipoprotein E knockout (ApoE KO) mice.
In understanding the mechanisms of cholesterol in the pathogenesis of atherosclerosis, previous studies from other laboratories have demonstrated that cholesterol crystals (CC) induce scavenger receptor CD36 expression and NLRP3-mediated inflammasome formation.
Increased expression of CD36 occurs in human atherosclerotic lesions, and CD36 knockout mice show reduced uptake of modified LDLs and reduced atherosclerosis.
Inflammation relevant genes, such as F4/80, tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, and monocyte chemoattractant protein (MCP)-1, and lipid metabolism associated gene, such as LDL receptor, class A scavenger receptors (SR-A), scavenger receptor class B type I (SR-BI), CD36, ATP binding cassette subfamily A member 1 (ABCA1), and ATP binding cassette subfamily G member 1 (ABCG1) in the aorta were significantly down-regulated in miR-217 group when compared with atherosclerosis group.
Macrophage foam cell formation by oxidized low-density lipoprotein (oxLDL) is a key step in the progression of atherosclerosis, which is involved in cholesterol influx and efflux in macrophages mediated by related proteins such as peroxisome proliferator-activated receptor γ (PPARγ), CD36, PPARα, liver-X receptor α (LXRα), and ATP-binding cassette transporter A1 (ABCA1).
Macrophage foam cell formation mediated by CD36 receptor dependent internalization of oxidized low-density lipoprotein (oxLDL) is an important hallmark of early atherosclerosis.
Macrophage scavenger receptors, such as CD36 and class A scavenger receptor (SR-A), have previously been thought to play a central role in foam cell formation and atherogenesis by mediating the uptake of oxidized LDL.In this issue of the JCI, Moore et al. report that Apoe mice deficient in either CD36 or SR-A did not have less atherosclerosis at the level of the aortic valve than did wild-type Apoe mice.
Macrophages play a central role in the pathogenesis of atherosclerosis by accumulating cholesterol through increased uptake of oxidized low-density lipoproteins by scavenger receptor CD36, leading to foam cell formation.
Moreover, the lesion size of atherosclerosis was smaller in dihydromyricetin-treated ApoE<sup>-/-</sup> mice compared with the vehicle-treated mice, and the protein expression of CD36, SR-A, ABCA1, ABCG1 and LXRα in aortas was modulated similar to that observed in THP-1-derived macrophages.
Our findings indicated that myricetin suppressed cholesterol accumulation in macrophage foam cells by inhibition of CD36-mediated ox-LDL uptake, and suggested myricetin may have an important therapeutic function for atherosclerosis.
Our results conclude that IL-34 facilitates foam cell formation by increasing CD36-mediated lipid uptake and suggest a potential new risk biomarker for atherosclerosis.
Our results inferred that the HSP/GR complex-mediated CD36 axis was involved in the regulation of atherosclerosis development in mice verified by Co-IP assay, EMSA, and Chip-PCR.
Protein Kinase Cθ Via Activating Transcription Factor 2-Mediated CD36 Expression and Foam Cell Formation of Ly6C<sup>hi</sup> Cells Contributes to Atherosclerosis.
Recent advances on the emerging role of CD36 and GHRP hexarelin in regulating PPARγ downstream actions with benefits on atherosclerosis, hepatic cholesterol biosynthesis and fat mitochondrial biogenesis are summarized here.
Recent literature has implicated CD36 in the pathogenesis of metabolic dysregulation such as found in obesity, insulin resistance, and atherosclerosis.