Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2492894 | Medical Hypotheses | 2006 | 6 Pages |
SummaryCurrent understanding of the pathophysiology of atherosclerosis has undergone a remarkable evolution. Compelling evidence has evolved at both the basic science and clinical level for the importance of inflammation in the pathogenesis of atherosclerosis and its complications. Recent research has shown that both systemic and local inflammation plays a central role in all phases of the atherosclerotic process. Inflammatory cells dominate early atherosclerotic lesions, inflammatory cytokines accelerate progression of the lesions, and activation of inflammation can elicit acute coronary syndromes. Robust clinical studies have affirmed that fibrates are anti-atherogenic and can improve the cardiovascular risk profile. Fibrates not only modulate the serum concentrations of triglyceride and cholesterol, but also inhibit systemic inflammatory statue and inflammatory response in vascular cells. Fibrates act anti-inflammatory effects in monocyte/macrophage, T lymphocyte, endothelial cells, vascular smooth muscle cells and adipocytes. Since atherosclerosis is now regarded as an inflammatory disease and those inflammatory cells play critical important roles in the initiation and development of atherosclerosis, we hypothesize that anti-atherogenic properties of fibrates may be largely due to their anti-inflammatory effects.