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Myocardial angiogenesis: its absence makes the growing heart founder

Gerald W Dorn1

  • 1Center for Molecular Cardiovascular Research, University of Cincinnati, Cincinnati, OH 45267-0839, USA. dorngw@ucmail.uc.edu

Cell Metabolism
|May 10, 2007
PubMed

Insights

Tumor growth requires new blood vessels (angiogenesis). In heart muscle, p53 protein blocks a key pathway for blood vessel formation, worsening cardiac hypertrophy and dysfunction.

Area of Science:

  • Cardiovascular Biology
  • Oncology
  • Molecular Medicine

Background:

  • Angiogenesis is critical for both normal tissue development and the growth of tumors.
  • Cardiac hypertrophy, an enlargement of the heart muscle, can lead to heart failure.
  • Hypoxia-inducible factor 1 (HIF-1) is a key regulator of angiogenesis.

Purpose of the Study:

  • To investigate the role of p53 in regulating angiogenesis within the context of cardiac hypertrophy.
  • To understand how p53 expression impacts neovascularization in pressure-overload cardiac hypertrophy models.
  • To determine the contribution of p53-mediated effects on angiogenesis to cardiac decompensation.

Main Methods:

  • Utilized a pressure-overload model of cardiac hypertrophy in animal studies.
  • Examined the expression levels of p53 and HIF-1 in hypertrophying heart muscle.
  • Assessed the impact of p53 on HIF-1-mediated neovascularization using molecular and histological techniques.

Main Results:

  • p53 expression was found to be elevated in hypertrophying heart muscle.
  • Increased p53 expression was associated with impaired HIF-1-mediated neovascularization.
  • The inhibition of neovascularization by p53 contributed to the functional decline of the overloaded heart.

Conclusions:

  • p53 acts as an inhibitor of angiogenesis in the hypertrophying heart.
  • The p53-mediated suppression of neovascularization exacerbates cardiac decompensation in pressure-overload hypertrophy.
  • Targeting p53 or related pathways may offer therapeutic strategies for heart failure associated with cardiac hypertrophy.

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