Absence of CD36 protects against atherosclerosis in ApoE knock-out mice with no additional protection provided by absence of scavenger receptor A I/II

Abstract

These results provide new insights into the pro-atherogenic mechanisms of CD36 by implicating processes other than modified lipoprotein uptake.

Inflammatory stress promotes lipid accumulation in the aorta and liver of SR-A/CD36 double knock-out mice

“…Decreased expression of cytokines indicate that the loss of SRs is associated with a reduction in the inflammation milieu. In agreement with this, Kuchibhotla et al (6) reported decreased serum levels of inflammation markers in ApoE -/-cd36 -/-Msr1 -/-mice, several of which overlap with our measurements of inflammation gene expression in the aortas.…”

“…However, other studies have revealed that the absence of SR-A was protective (32% decrease in the lesion). The combined absence of CD36 and SR-A provided no further protection in individuals of either gender (6).…”

D4F alleviates macrophage-derived foam cell apoptosis by inhibiting CD36 expression and ER stress-CHOP pathway

“…Numerous experimental fi ndings, including our own, have revealed that accumulation of intracellular cholesterol is an important inducer of ER stress and macrophage apoptosis in vivo and in vitro (33)(34)(35). CD36, a class B scavenger receptor, plays a quantitatively crucial role in ox-LDL uptake and cholesterol accumulation in macrophages, whereas suppression of CD36 expression is able to significantly decrease the ability of macrophages to accumulate ox-LDL and reduce the development of atherosclerosis, suggesting that it could be an important target for therapeutic treatment ( 27,36,37 ). Our recent study indicated that CD36-mediated ox-LDL uptake in macrophages triggered ER stress response (ATF6, inositol-requiring kinase/endonuclease-1, and GRP78), which, in turn, played a critical role in CD36 upregulation and then enhanced the foam cell formation by promoting uptake of ox-LDL, indicating that there may be a positive feedback loop between ER stress and CD36 expression ( 27 ).…”

Collagens in the progression and complications of atherosclerosis

“…Furthermore, contradictory data on the importance of the SRA in mediating plaque growth arises from studies of ApoE-null mice with gene deletions for SRA, and may be related to the use of mice with different genetic backgrounds. [68][69][70] Recent research has shown that DDRs play important roles in the activation and differentiation of macrophages. DDR1 mRNA and protein was detected on cultured PBMCs and polymorphonuclear leukocytes (PMNs), and was upregulated by stimulation with IL-1, TNFα, and LPS.…”