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Updated: Aug 22, 2026

Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Lesion progression and plaque composition are not altered in older apoE-/- mice lacking tumor necrosis factor-alpha
Erwin Blessing1, Florian Bea, Cho-chou Kuo
1Department of Pathobiology, University of Washington, P.O. Box 353410, Seattle, WA 98195, USA.
Background:
Inflammatory processes are an integral component of the initiation, progression, and destabilization of atherosclerotic lesions. Tumor necrosis factor-alpha (TNF-alpha) is considered a primary mediator of inflammatory processes.
Methods And Results:
The role of TNF-alpha in plaque progression and plaque destabilization was investigated in the innominate arteries of older TNF-alpha receptor p55 deficient mice that were generated on a hyperlipidemic apolipoprotein E deficient background (p55-/- apoE-/-). There were no significant differences in levels of circulating cytokines, plaque progression, plaque composition or features of plaque destabilization in p55-/- apoE-/- compared to wild type (p55+/+ apoE-/-) mice.
Conclusions:
Progression and destabilization of advanced atherosclerotic lesions does not seem to be mediated via the TNF-alpha receptor p55.
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