The tissue-specific distribution of these receptors critically influences their pathological roles in atherosclerosis: SR-A and CD36 in macrophages contribute to foam cell formation, LOX-1 in endothelial cells upregulates adhesion molecules such as VCAM-1 and ICAM-1 to recruit monocytes, and SR-A in VSMCs promotes fibrous cap disruption [153]. The gene discussed is SRA1; the disease is atherosclerosis.