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Proteasome inhibitors reduce thrombospondin-1 release in human dysferlin-deficient myotubes.

Esther Fernández-SimónCinta LleixàXavier Suarez-CalvetJordi Diaz-ManeraIsabel IllaEduard GallardoNoemi de Luna
Published in: BMC musculoskeletal disorders (2020)
Our findings indicate that the ubiquitin-proteasome system might not be the main mechanism of mutant dysferlin degradation. However, its inhibition could help to improve muscle inflammation by reducing TSP-1 release.
Keyphrases
  • endothelial cells
  • oxidative stress
  • wild type
  • skeletal muscle
  • induced pluripotent stem cells