Control of cell proliferation in atherosclerosis: insights from animal models and human studies

Cardiovasc Res. 2010 May 1;86(2):254-64. doi: 10.1093/cvr/cvp363. Epub 2009 Nov 9.


Excessive hyperplastic cell growth within occlusive vascular lesions has been recognized as a key component of the inflammatory response associated with atherosclerosis, restenosis post-angioplasty, and graft atherosclerosis after coronary artery bypass. Understanding the molecular mechanisms that regulate arterial cell proliferation is therefore essential for the development of new tools for the treatment of these diseases. Mammalian cell proliferation is controlled by a large number of proteins that modulate the mitotic cell cycle, including cyclin-dependent kinases, cyclins, and tumour suppressors. The purpose of this review is to summarize current knowledge about the role of these cell cycle regulators in the development of native and graft atherosclerosis that has arisen from animal studies, histological examination of specimens from human patients, and genetic studies.

Publication types

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

MeSH terms

  • Animals
  • Atherosclerosis / genetics
  • Atherosclerosis / metabolism
  • Atherosclerosis / pathology*
  • Blood Vessels / metabolism
  • Blood Vessels / pathology*
  • Cell Cycle Proteins / metabolism
  • Cell Cycle* / genetics
  • Cell Proliferation*
  • Disease Models, Animal
  • Humans
  • Hyperplasia
  • Inflammation / genetics
  • Inflammation / metabolism
  • Inflammation / pathology*


  • Cell Cycle Proteins