Proliferation and the monoclonal origins of atherosclerotic lesions

Annu Rev Med. 1998;49:437-60. doi: 10.1146/annurev.med.49.1.437.

Abstract

Benditt's observation of the monoclonal origin of the atherosclerotic lesion has been controversial because it appeared to conflict with conventional wisdom. A new method based on a polymerase chain reaction amplification of the DNA of an X-inactivated gene from microdissected tissue confirms that Benditt was correct. However, this monoclonal expansion can also be found in nonatherosclerotic intima and media. These new data suggest that plaque clonality may represent expansion of preexisting patches of cells arising during development of the media. This developmental view does not conflict with other recent evidence that plaque expansion is associated with mutation or viral events. However, if plaques arise from patches, then early developmental mechanisms may be critical to the later evolution of the lesions.

Publication types

  • Review

MeSH terms

  • Arteriosclerosis / genetics
  • Arteriosclerosis / pathology*
  • Arteriosclerosis / virology
  • Cell Division / genetics
  • Cell Lineage / genetics
  • Clone Cells / pathology
  • DNA / genetics
  • Gene Expression / genetics
  • Gene Expression Regulation, Viral
  • Humans
  • Muscle, Smooth, Vascular / pathology
  • Mutation / genetics
  • Polymerase Chain Reaction
  • Tunica Intima / pathology
  • Tunica Media / pathology
  • Virus Diseases / genetics
  • Virus Diseases / pathology

Substances

  • DNA