Adhesion proteins, stem cells, and arrhythmogenesis

Cardiovasc Toxicol. 2008 Mar;8(1):1-13. doi: 10.1007/s12012-007-9008-5. Epub 2008 Jan 5.

Abstract

Cell-transplantation therapy is a promising treatment option that is being actively explored as a way to repair cardiac muscle. The ultimate goal is to reconstitute the architecture of the cardiac muscle and to reestablish electrical propagation, while avoiding hypertrophy and scar formation. In this review, we focus on recent advances in the field as well as the difficulties encountered when the engraftment of cells into the host tissue is to be confirmed and functionally characterized. This is critical since incomplete or partial engraftment of transplanted cells within the host cardiac network exacerbates the heterogeneity already present in the injured myocardium and increases its propensity to arrhythmia. We conclude with a brief discussion of how the modulation of cell adhesion via modification of coupling proteins within transplanted cells may facilitate engraftment and alleviate the arrhythmogenic potential of cardiac grafts.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Arrhythmias, Cardiac / metabolism
  • Arrhythmias, Cardiac / physiopathology*
  • Cell Adhesion Molecules / physiology*
  • Disease Models, Animal
  • Heart / physiology*
  • Humans
  • Myoblasts, Cardiac / physiology*
  • Myocardial Ischemia / metabolism
  • Myocardial Ischemia / physiopathology
  • Myocardial Ischemia / therapy
  • Myocytes, Cardiac
  • Stem Cell Transplantation*
  • Tissue Engineering

Substances

  • Cell Adhesion Molecules