Salicylates and vascular smooth muscle cell proliferation: molecular mechanisms for cell cycle arrest

Trends Cardiovasc Med. 2001 Nov;11(8):339-44. doi: 10.1016/s1050-1738(01)00133-5.

Abstract

Salicylates are effective prophylactic treatment strategies for myocardial infarction and ischemic strokes. Recent evidence suggests that high doses of salicylates may exert direct, platelet-independent effects on the vascular wall. Salicylate and aspirin, in concentrations between 1 and 5 mM, effectively inhibit vascular smooth muscle cell proliferation and DNA synthesis without inducing cellular toxicity or apoptosis. This inhibition is associated with effects on specific cell-cycle regulatory molecules, and may proceed via downregulation of the transcription factor, nuclear factor (NF)-kappaB. High-dose salicylates and selective NF-kappaB inhibitors may, therefore, play an important role in the management of vascular proliferative disorders.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Aspirin / pharmacology
  • Cell Cycle / drug effects*
  • Cell Division / drug effects
  • Down-Regulation
  • Humans
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / drug effects*
  • Muscle, Smooth, Vascular / metabolism
  • NF-kappa B / drug effects
  • NF-kappa B / physiology
  • Salicylates / pharmacology*

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • NF-kappa B
  • Salicylates
  • Aspirin