Myostatin represses physiological hypertrophy of the heart and excitation-contraction coupling

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Buel D Rodgers1, Jillian P Interlichia, Dilip K Garikipati

  • 1Department of Animal Sciences and School of Molecular Biosciences, Washington State University, Pullman, WA 99164, USA. danrodgers@wsu.edu

The Journal of Physiology
|September 9, 2009
PubMed

Insights

Myostatin inhibits cardiac muscle growth and function. Its inhibition may promote physiological cardiac hypertrophy, potentially aiding in the repair of damaged heart muscle.

Area of Science:

  • Cardiovascular Biology
  • Muscle Physiology
  • Molecular Regulation

Background:

  • Myostatin is a known negative regulator of skeletal muscle growth.
  • The role of myostatin in cardiac muscle physiology and growth remains largely unexplored.

Purpose of the Study:

  • To investigate the function of myostatin in cardiac muscle.
  • To determine myostatin's effect on cardiac cell proliferation, differentiation, and excitation-contraction coupling.
  • To assess the impact of myostatin deficiency on cardiac function and response to beta-adrenergic stimulation.

Main Methods:

  • Investigated myostatin's role in basal and IGF-1-stimulated cardiomyocyte proliferation and differentiation.
  • Analyzed the effects of myostatin deficiency on cardiac excitation-contraction (EC) coupling and myocyte contractility.
  • Assessed cardiac output and beta-adrenergic responsiveness in myostatin-null mice in vivo.
  • Measured force and ATPase activity to evaluate myofilament function.

Main Results:

  • Myostatin inhibits basal and IGF-1-stimulated cardiomyocyte proliferation and differentiation.
  • Loss of myostatin leads to eccentric cardiac hypertrophy and enhanced responsiveness to beta-adrenergic stimulation.
  • Myostatin-null ventricular myocytes exhibit larger intracellular calcium ([Ca(2+)](i)) transients and contractions.
  • Enhanced cardiac output in myostatin-null mice is attributed to increased SR Ca(2+) release during EC coupling and physiological hypertrophy.

Conclusions:

  • Myostatin acts as a repressor of physiological cardiac muscle growth and function.
  • Controlled inhibition of myostatin could be a therapeutic strategy for cardiac repair by inducing physiological hypertrophy.

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