How an artery heals - PubMed (original) (raw)

The central role of cholesterol-rich, apoB-lipoproteins in atherosclerosis initiation, progression, and regression.

Panel A

: Initiation and progression of atherosclerosis. Arrows are color coded to indicate crucial mechanisms in the retention of cholesterol-rich apoB-lipoproteins within the arterial wall, which is the key initiating step in atherogenesis (yellow); and then maladaptive local responses to the retained and modified lipoproteins that lead to plaque growth and evolution (red).

Panel B

: Plaque stabilization, resolution of maladaptive sterile inflammation, and atherosclerosis regression. Drastic improvements in the plasma lipoprotein profile allow arterial healing. Shown schematically are vast reductions in circulating concentrations of apoB-lipoproteins combined with an increase in functional HDL and other putative acceptors of exchangeable material from the plaque. The green arrows indicate previously reported mechanisms for resolution of an established plaque. The two green Xs indicate new mechanisms found by Bartels, Christoffersen, et al. – namely, an improved endothelial barrier to LDL and a drop in the fractional degradation of LDL that enters the plaque during early regression. Abbreviations: ABC, ATP-binding cassette transporters; apoA-I, apolipoprotein A-I; AqD, aqueous diffusion; ChEase, cholesteryl esterase; IDL, intermediate-density lipoprotein; IFN-γ, interferon γ; IL-4, interleukin 4; LP, lipoprotein; LpL, lipoprotein lipase; MMPs, matrix metalloproteinases; MPs, macrophages; PC, phosphatidylcholine; PGs, proteoglycans; Remnant, cholesterol-rich apoB-containing remnant lipoprotein; SMase, secretory sphingomyelinase; SMC, smooth muscle cell; SRBI, scavenger receptor class B type I; TF, tissue factor; UC, unesterified cholesterol. Adapted from reference with permission.