BMS 460 Lecture Notes - Icam-1, Endothelial Dysfunction, Angioplasty
26 Apr 2014
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Document Summary
Fatty streaks are a collection of foamy macrophages in the intima. Sequence of atherosclerotic plaque development over decades its natural history. Injury to ec from a variety of insults causes loss of normal anithrombotic and vasodilator cytokines. Inflammatory cytokines (tnf- ; interferon and interleukin-1) plus other factors such as oxygen radicals. Growth factors are released in inflammation: angiotensin ii, fgf, pdgf which stimulate. Macrophages adhere to injured ec"s via adhesion molecules such as vcam and invade wall (foam cells) Macrophages release enzymes and oxygen radicals oxidize the ldl and further injure vessel wall. Evolution of a plaque from injury by ox-ldl all the way to complicated plaque with calcifications. Local cytokine activity stimulated by oxidative stress of oxidized ldl. Macrophage migration across wall (m-csf) and expression of scavenger receptors. Vsmc elaborate extracellular matrix (fatty streak to fibrous plaque) Oxidized ldl causes adhesion and entry of monocytes and t lymphocytes across endothelium.
