Cytokines and smooth muscle cells in atherosclerosis.

For several years it has been recognised that the common denominator for many of the well known risk factors for cardiovascular disease is that they all may give rise to chronic inflammatory reactions in vascular tissues. New tools made available through rapid progress in the fields of immunology and molecular biology have made it possible to reach a better understanding of the molecular events leading to the development of atherosclerosis. These developments have resulted in a renewed interest in the role of inflammatory and immune reactions in atherogenesis. During recent years it has also become increasingly clear that the release and ability to respond to cytokines is not restricted to the cells classically included in the immune system. At least in vitro, smooth muscle cells and endothelial cells produce and respond to cytokines in a manner suggesting that they play active roles in inflammatory reactions. Several cytokines have been found to influence the growth of smooth muscle cells, suggesting a possible link between two of the major characteristics of atherosclerotic lesions: the inflammatory reaction, and the intimal proliferation of smooth muscle cells. Of particular interest is the ability of interleukin-1 and TGF beta to induce autocrine PDGF loops in smooth muscle cells. By this mechanism a transient secretion of cytokines from activated leucocytes may give rise to prolonged activation of smooth muscle cell proliferation. However, the effects of cytokines on vascular cells are very complex and it cannot be taken for granted that the inflammatory reaction generally encountered in atherosclerotic lesions only serves to promote the progress of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)