There are experimental data that demonstrate that eicosanoids derived from the arterial wall serve to maintain the cell in a contractile, quiescent, phenotypic state, which is responsive to vasoactive stimuli and not responsive to mitogens. Furthermore, endogenously synthesized eicosanoids help to maintain cellular cholesterol content at a low level. However, eicosanoids derived from monocytes and neutrophils may promote the inflammatory response by promoting smooth muscle cell modulation to the synthetic phenotype and promoting smooth muscle cell migration, proliferation, and cholesteryl ester deposition. This raises the possibility that mural eicosanoids are antiatherogenic, while eicosanoids derived from inflammatory cells may initiate or mediate the processes leading to plaque development. The data are summarized in Table 1.
CITATION STYLE
Pomerantz, K. B., & Hajjar, D. P. (1989). Eicosanoids in regulation of arterial smooth muscle cell phenotype, proliferative capacity, and cholesterol metabolism. Arteriosclerosis. https://doi.org/10.1161/01.atv.9.4.413
Mendeley helps you to discover research relevant for your work.