Thus, targeting to CD36 and its downstream effectors may serve as potential new strategies against chronic inflammatory diseases such as atherosclerosis.
Functionally, MT4-MMP-null Mafb+AIM+ peritoneal macrophages express higher AIM and scavenger receptor CD36, are more resistant to apoptosis, and bind acLDL avidly, all of which contribute to atherosclerosis.
We found that allergic asthma increased the expression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) in the liver and CD36 in the aorta during the acute and advanced stages of atherosclerosis, respectively.
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.
The scavenger protein CD36 has been shown to play a substantial role in the pathogenesis of atherosclerosis, largely through its interaction with oxidised LDL.
The blocking of autophagy-lysosome induction could increase CD36 protein level, foam-cell formation, and migration, thus abolishing the protective effects of CTRP13 on atherosclerosis.
The aim of this study was to investigate the mechanisms through which quercetin protects against atherosclerosis (AS) in apoE‑/‑ mice by regulating the expression of proprotein convertase subtilisin/kexin type 9 (PCSK9), cluster of differentiation 36 (CD36), peroxisome proliferator‑activated receptor γ (PPARγ), liver X receptor α (LXRα) and ATP binding cassette transporter A1 (ABCA1).
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.
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.
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.
Because CD36 is an essential component of atherosclerosis, defining the function of CD36 and its corresponding signaling pathway may lead to a new treatment strategy for atherosclerosis.
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.
Accordingly, paeonol retarded the progress of atherosclerosis in ApoE(‑/‑) mice and modulated the expression of CD36 and ABCA1 in aortas similarly to that observed in macrophages.
We report here that the PPARgamma-specific agonists rosiglitazone and GW7845 strongly inhibited the development of atherosclerosis in LDL receptor-deficient male mice, despite increased expression of the CD36 scavenger receptor in the arterial wall.
This is the first established link between physical binding of fatty acids and a function of CD36, and has implications for obesity and atherosclerosis.
These results identify such enhanced CD36 expression as a novel nicotine-mediated pathway that may constitute an independent risk factor for atherosclerosis in smokers.
This review addresses the regulation and potential role of CD36 in macrophage foam cell formation and atherosclerosis, with particular emphasis on the mechanisms by which CD36 expression is altered in response to lipid modulation of peroxisome proliferator-activated receptor gamma signaling.