High CO₂ Downregulates Skeletal Muscle Protein Anabolism via AMP-activated Protein Kinase α2-mediated Depressed Ribosomal Biogenesis.

ABSTRACT: High CO₂ retention, or hypercapnia, is associated with worse outcomes in patients with chronic pulmonary diseases. Skeletal muscle wasting is also an independent predictor of poor outcomes in patients with acute and chronic pulmonary diseases. Although previous evidence indicates that high CO₂ accelerates skeletal muscle catabolism via AMPK (AMP-activated protein kinase)-FoxO3a-MuRF1 (E3-ubiquitin ligase muscle RING finger protein 1), little is known about the role of high CO₂ in regulating skeletal muscle anabolism. In the present study, we investigated the potential role of high CO₂ in attenuating skeletal muscle protein synthesis. We found that locomotor muscles from patients with chronic CO₂ retention demonstrated depressed ribosom

SUBMITTER: Korponay TC 

PROVIDER: S-EPMC6938128 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature