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Retinoid-dependent pathways suppress myocardial cell hypertrophy

M D Zhou1, H M Sucov, R M Evans

  • 1Department of Medicine, University of California, San Diego, School of Medicine, La Jolla 92093, USA.

Proceedings of the National Academy of Sciences of the United States of America
|August 1, 1995
PubMed

Insights

Retinoic acid (RA) suppresses cardiac hypertrophy by inhibiting alpha-adrenergic receptor pathways. This RA-mediated suppression, involving RAR/RXR heterodimers, offers potential therapeutic strategies for heart conditions.

Area of Science:

  • Cardiovascular Biology
  • Molecular Endocrinology
  • Cellular Signaling

Background:

  • Cardiac hypertrophy is a significant risk factor for heart failure.
  • Alpha-adrenergic receptor agonists are known inducers of cardiac hypertrophy.
  • Retinoid signaling pathways play crucial roles in cellular development and function.

Purpose of the Study:

  • To investigate the role of retinoic acid (RA) in modulating cardiac muscle cell hypertrophy.
  • To identify the specific signaling pathways involved in RA-mediated suppression of hypertrophy.
  • To explore the potential therapeutic implications of RA signaling in cardiovascular disease.

Main Methods:

  • Utilized an in vitro model of cardiac muscle cell hypertrophy.
  • Administered phenylephrine (alpha-adrenergic agonist) and retinoic acid (RA).
  • Performed transient transfection assays to analyze retinoic acid receptor (RAR/RXR) activity.

Main Results:

  • Physiological concentrations of RA suppressed phenylephrine-induced increases in cell size and atrial natriuretic factor (ANF) gene expression.
  • RA selectively inhibited alpha-adrenergic receptor-dependent hypertrophy, but not serum-induced hypertrophy.
  • Data indicated that RAR/RXR heterodimers mediate the suppression of alpha-adrenergic receptor-dependent hypertrophy.

Conclusions:

  • A retinoic acid (RA)-mediated pathway suppresses key features of cardiac hypertrophy induced by alpha-adrenergic stimulation.
  • RAR/RXR heterodimers are crucial for this suppressive effect.
  • These findings suggest a potential in vivo therapeutic pathway for managing cardiac hypertrophy.

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