Succinate Dehydrogenase (SDH)-subunit C regulates muscle oxygen consumption and fatigability in an animal model of pulmonary emphysema.

Using a recently established animal model of pulmonary emphysema-driven skeletal muscle dysfunction, we found downregulation of succinate dehydrogenase subunit C in association with lower oxygen consumption and fatigue-tolerance in locomotor muscles



Scholarcy highlights

  • Patients with chronic obstructive pulmonary disease often develop locomotor muscle dysfunction, which entails atrophy and reduced force-generation capacity
  • This led to a substantial decrease in oxygen consumption rate, supporting the hypothesis that SDHC downregulation in-vivo could be partially responsible for the metabolic and functional phenotype observed in emphysema mouse muscles
  • This strongly suggests that SDHC downregulation is, at least partially, responsible for muscle metabolic dysfunction seen in this model of pulmonary emphysema
  • While most of the research conducted in the field of COPD-associated muscle dysfunction has so far focused on the conspicuous reduction of muscle mass, to our knowledge this is the first mechanistic study that disaggregates the investigation of muscle metabolic properties in the context of pulmonary emphysema
  • We have shown that there are no significant baseline differences between fiber types in extensor digitorum longus muscle from IL13TG and IL13TG and wild-type mice, yet overexpression of SDHC leads to larger number of types 2A and 2X fibers suggesting that muscle fiber type profile could be regulated by SDHC independently of its succinate dehydrogenase complex enzymatic function
  • Succinate dehydrogenase subunit C overexpression abrogates reduced oxygen consumption and fatigue-tolerance observed in an animal model of pulmonary emphysemainduced skeletal muscle dysfunction, which is associated with an increase in relatively more oxidative type 2A and X fibers

Need more features? Save interactive summary cards to your Scholarcy Library.