Abstract
Atherosclerosis is a disease of the arterial wall that is modulated by the inflammatory balance. Transforming growth factor [TGF] type β1, β2, and β3 are cytokines with broad activities on cells and tissues in the cardiovascular system and have been proposed to play a role in the pathogenesis of atherosclerosis. This cytokine is a major orchestrator of the fibroproliferative response to tissue damage. In fact, besides its effects on cell cycle regulation and survival/apoptosis in many cell types including endothelial and smooth muscle cells, TGF-β is an important antiinflammatory cytokine. Although we might be tempted to label TGF-β as either an “atheroprotective” or “atherogenic” factor, TGF-β is more likely to play a central role in both normal and pathological vascular repair.
Highlights
Atherosclerosis has been designed as an inflammatory disease of the arterial wall [1]
Many results suggest that anti-inflammatory cytokines with deactivating properties on macrophages and/or T cells are produced within the atherosclerotic lesion [3,4,5,6]
The role of TGF-β and SMAD signalling in atherogenesis and vascular inflammation has previously been reviewed by Feinberg and Jain [8]
Summary
Atherosclerosis has been designed as an inflammatory disease of the arterial wall [1]. Endothelial activation by oxidized lipoproteins plays an important role in the initiation of the atherosclerotic lesion through increased adhesion of mononuclear cells and their recruitment into the vascular wall [1]. It was demonstrated that the recruited inflammatory cells induce inflammatory cytokines and chemokines expression, enhancing lesion progression.
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