Myostatin does not regulate cardiac hypertrophy or fibrosis

Ronald D. Cohn, Hsin Yueh Liang, Reena Shetty, Theodore Abraham, Kathryn R. Wagner

Research output: Contribution to journalArticlepeer-review

Abstract

Myostatin is a negative regulator of muscle growth. Loss of myostatin has been shown to cause increase in skeletal muscle size and improve skeletal muscle function and fibrosis in the dystrophin-deficient mdx muscular dystrophy mouse model. We evaluated whether lack of myostatin has an impact on cardiac muscle growth and fibrosis in vivo. Using genetically modified mice we assessed whether myostatin absence induces similar beneficial effects on cardiac function and fibrosis. Cardiac mass and ejection fraction were measured in wild-type, myostatin-null, mdx and double mutant mdx/myostatin-null mice by high resolution echocardiography. Heart mass, myocyte area and extent of cardiac fibrosis were determined post mortem. Myostatin-null mice do not demonstrate ventricular hypertrophy when compared to wild-type mice as shown by echocardiography (ventricular mass 0.69 ± 0.01 vs. 0.69 ± 0.018 g) and morphometric analyses including heart/body weight ratio (5.39 ± 0.45 vs. 5.62 ± 0.58 mg/g) and cardiomyocyte area 113.67 ± 1.5, 116.85 ± 1.9 μm2). Moreover, absence of myostatin does not attenuate cardiac fibrosis in the dystrophin-deficient mdx mouse (12.2% vs. 12%). The physiological role of myostatin in cardiac muscle appears significantly different than that in skeletal muscle as it does not induce cardiac hypertrophy and does not modulate cardiac fibrosis in mdx mice.

Original languageEnglish (US)
Pages (from-to)290-296
Number of pages7
JournalNeuromuscular Disorders
Volume17
Issue number4
DOIs
StatePublished - Apr 2007

Keywords

  • Cardiomyopathy
  • Duchenne muscular dystrophy
  • Myostatin

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Neurology
  • Clinical Neurology
  • Genetics(clinical)

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