Failure of the ryanodine receptor causes myocardial senescence and fibrosis in DMD

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Researchers in the south of France have studied the determinants of the degeneration and fibrosis observed in cardiomyopathy linked to Duchenne muscular dystrophy (DMD) in animals and humans:

  • human pluripotent stem cells from DMD patients were first transformed into cardiomyocytes,
  • myocardial tissue from DMD model dogs (GRMD) was also analysed,
  • dysfunction of the type 2 ryanodine receptor and disruption of calcium flow appear to be at the root of fibrosis and myocardial senescence.

The researchers were also able to demonstrate the value of a molecule (S107) in stabilising the phenomenon and improving the phenotype.

 

Ryanodine receptor dysfunction causes senescence and fibrosis in Duchenne dilated cardiomyopathy. Souidi M, Resta J, Dridi H et al. J Cachexia Sarcopenia Muscle. 2024 Janv.

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