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. Author manuscript; available in PMC: 2010 Feb 22.
Published in final edited form as: Nature. 2000 Sep 14;407(6801):233–241. doi: 10.1038/35025203

Figure 6.

Figure 6

Formation of fibrous plaques. A number of risk factors, including elevated levels of homocysteine and angiotensin II (produced through the action of angiotensin-converting enzyme, ACE), stimulate the migration or proliferation of SMCs. Oestrogens exert beneficial effects on plasma lipoprotein levels and they also stimulate production of NO and prostacyclin by endothelial cells. The interaction of CD40 and CD40 ligand (CD40L) stimulates T lymphocytes (T cells) and macrophages to express cytokines such as IFN-γ that can influence inflammation, SMC growth and matrix accumulation. The intimal SMCs secrete extracellular matrix and give rise to a fibrous cap.