Reveals that targeting SR-A and CD36 reduces lesion complexity in hyperlipidemic mice, suggesting a pathway to improve plaque stability.
Although targeted deletion of SR-A and CD36 does not abrogate macrophage foam cell formation or substantially reduce atherosclerotic lesion area in Apoe(-/-) mice, loss of these pathways does reduce progression to more advanced necrotic lesions. These data suggest that targeted inhibition of these pathways in vivo may reduce lesional inflammation and promote plaque stability.
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Manning-Tobin et al. (2008) studied this question.
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