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Review
. 1995 May;15(5):551-61.
doi: 10.1161/01.atv.15.5.551.

The response-to-retention hypothesis of early atherogenesis

K J Williams  1 , I Tabas
Affiliations
Review

The response-to-retention hypothesis of early atherogenesis

K J Williams et al. Arterioscler Thromb Vasc Biol. 1995 May.
No abstract available

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Figures

Figure 1
Figure 1
Schematic of the response-to-retention model of early atherogenesis. Mild to moderate hyperlipidemia causes lesion development only in specific sites within the arterial tree, implying the existence of predisposing stimuli, such as sheer stress, that make these sites particularly lesion-prone by stimulating local synthesis of apoB-retentive molecules (B). Predisposing stimuli in the absence of abundant atherogenic lipoproteins (ie, <2 mmol LDL cholesterol/L) are insufficient to cause atherogenesis. Predisposing stimuli in the presence of abundant atherogenic lipoproteins result in lipoprotein retention (C). Evidence suggests that aggregation promptly follows or may be part of the retentive process. Once significant retention has occurred, a cascade of early responses, including lipoprotein oxidation and cellular chemotaxis, leads to lesion development (D). ECs indicates endothelial cells; PGs, proteoglycans; IEL, internal elastic lamina; SMCs, smooth muscle cells; LpL, lipoprotein lipase; SMase, sphingomyelinase; and LPs, lipoproteins.
See this image and copyright information in PMC

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