A cascade model for restenosis: A special case of atherosclerosis progression Review uri icon

Overview

MeSH Major

  • Arteriosclerosis

abstract

  • Several experimental observations support this novel mechanistic model. Leukocytes and smooth muscle cells express genes for cytokines and growth factors, and products of coagulation and thrombosis can activate mononuclear phagocytes. Cytokines and growth factors often augment their own gene expression and induce one another, providing a potential intralesional amplification loop. Experimental atheroma and advanced human atherosclerotic lesions do not express high levels of growth-stimulatory cytokines such as interleukin-1 or tumor necrosis factor in the basal state but exhibit inducible expression in response to an injurious stimulus. Thus, cascades of autocrine or paracrine mediators whose expression is triggered by vascular injury might contribute to deranged smooth muscle behavior during restenosis.

publication date

  • January 1992

Research

keywords

  • Review

Identity

Language

  • eng

PubMed ID

  • 1424051

Additional Document Info

start page

  • III47

end page

  • 52

volume

  • 86

number

  • 6 SUPPL.