The inflammation hypothesis and its potential relevance to statin therapy

Am J Cardiol. 2007 Mar 1;99(5):732-8. doi: 10.1016/j.amjcard.2006.09.125. Epub 2007 Jan 10.

Abstract

Inflammatory cytokines have a central role in atherogenesis and plaque rupture. These mediators, including tumor necrosis factor, interleukins, and matrix metalloproteinases and transforming growth factor-beta are also prominent in other chronic progressive diseases characterized by cell apoptosis and tissue fibrosis. This review extends the inflammation hypothesis to critical analysis of studies to bearing on the role of inflammation in chronic conditions that commonly accompany coronary disease. Because statins inhibit the expression of inflammatory mediators, the review then analyzes the laboratory and clinical data that may justify trials of statins in nonatherosclerotic disease. In conclusion, despite far different clinical presentations, chronic progressive diseases characterized by apoptosis and fibrosis have persistence of inflammatory cytokines as a final common pathway, and thus may benefit from the pleiotropic effects of statin therapy.

Publication types

  • Review

MeSH terms

  • Chronic Disease
  • Cytokines / drug effects
  • Cytokines / physiology*
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
  • Inflammation / etiology*
  • Inflammation / pathology
  • Inflammation / physiopathology

Substances

  • Cytokines
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors