Early origins of heart disease: low birth weight and determinants of cardiomyocyte endowment

Clin Exp Pharmacol Physiol. 2012 Sep;39(9):814-23. doi: 10.1111/j.1440-1681.2011.05649.x.

Abstract

1. World-wide epidemiological and experimental animal studies demonstrate that adversity in fetal life, resulting in intrauterine growth restriction, programmes the offspring for a greater susceptibility to ischaemic heart disease and heart failure in adult life. 2. After cardiogenesis, cardiomyocyte endowment is determined by a range of hormones and signalling pathways that regulate cardiomyocyte proliferation, apoptosis and the timing of multinucleation/terminal differentiation. 3. The small fetus may have reduced cardiomyocyte endowment owing to the impact of a suboptimal intrauterine environment on the signalling pathways that regulate cardiomyocyte proliferation, apoptosis and the timing of terminal differentiation.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis
  • Cell Proliferation
  • Disease Susceptibility
  • Female
  • Fetal Growth Retardation / genetics
  • Fetal Growth Retardation / pathology
  • Fetal Growth Retardation / physiopathology*
  • Heart / embryology*
  • Heart / physiopathology
  • Heart Diseases / etiology*
  • Heart Diseases / genetics
  • Heart Diseases / pathology
  • Heart Diseases / physiopathology
  • Humans
  • Male
  • Myocytes, Cardiac / pathology*
  • Organogenesis*
  • Polyploidy
  • Pregnancy
  • Species Specificity