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Lipids and Pathogenesis

In coronary disease, accumulation of lipids along blood vessel walls progresses into characteristic lesions that are hallmarks of the disease process. Lee et al. (see the Perspective by Plutzky) show that the inflammatory response associated with atherogenesis may hinge on a nuclear receptor called PPARδ that is expressed in macrophages. PPARδ appears to control the expression of proinflammatory genes in mouse macrophages, and its absence in mice caused a reduction in lesions by about 60%. This nuclear receptor may thus act as a molecular switch of the inflammatory program in macrophages and may represent a key target point for controlling disease progression. C.-H. Lee, A. Chawla, N. Urbiztondo, D. Liao, W. A. Boisvert, R. M. Evans, Transcriptional repression of atherogenic inflammation: Modulation by PPARδ. Science 302, 453-457 (2003). [Abstract] [Full Text] J. Plutzky, PPARs as therapeutic targets: Reverse cardiology? Science 302, 406-407 (2003). [Summary] [Full Text]