In atherosclerosis, increased LDL in monocyte macrophage due to
Atherosclerosis is characterized by the presence of intimal lesions called atheromas (or atheromatous or atherosclerotic plaques). Atheromatous plaques are raised lesions composed of soft grumous lipid cores (mainly cholesterol and cholesterol esters, with necrotic debris) covered by fibrous caps. atherosclerosis results from the following pathogenic events: * Endothelial injury--and resultant endothelial dysfunction--leading to increased permeability, leukocyte adhesion, and thrombosis * Accumulation of lipoproteins (mainly oxidized LDL and cholesterol crystals) in the vessel wall * Platelet adhesion * Monocyte adhesion to the endothelium, migration into the intima, and differentiation into macrophages and foam cells * Lipid accumulation within macrophages, which release inflammatory cytokines * Smooth muscle cell recruitment due to factors released from activated platelets, macrophages, and vascular wall cells * Smooth muscle cell proliferation and ECM production (Robbins basic pathology,9th edition.pg no.338)
LDL receptors on macrophage
LDL receptors on endothelium
Lipids in LDL get oxidized
All of the above
Cardiovascular system