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Muscle NAD + depletion and Serpina3n as molecular determinants of murine cancer cachexia—the effects of blocking myostatin and activins

Authors
  • Hulmi, J.J.1, 2
  • Penna, F.3
  • Pöllänen, N.4
  • Nissinen, T.A.1
  • Hentilä, J.1
  • Euro, L.5
  • Lautaoja, J.H.1
  • Ballarò, R.3
  • Soliymani, R.6
  • Baumann, M.6
  • Ritvos, O.2
  • Pirinen, E.4
  • Lalowski, M.6
  • 1 Faculty of Sport and Health Sciences, NeuroMuscular Research Center, University of Jyväskylä, Jyväskylä, Finland
  • 2 Department of Physiology, Faculty of Medicine, University of Helsinki, Helsinki, Finland
  • 3 Department of Clinical and Biological Sciences, University of Turin, Turin, Italy
  • 4 Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of Helsinki, Helsinki, Finland
  • 5 Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland
  • 6 Meilahti Clinical Proteomics Core Facility, HiLIFE, Faculty of Medicine, Biochemistry and Developmental biology, University of Helsinki, Helsinki, Finland
Type
Published Article
Journal
Molecular Metabolism
Publisher
Elsevier BV
Publication Date
Jun 26, 2020
Volume
41
Identifiers
DOI: 10.1016/j.molmet.2020.101046
PMID: 32599075
PMCID: PMC7364159
Source
PubMed Central
Keywords
License
Unknown

Abstract

• Cachectic muscle proteome shows decreased OXPHOS and increased acute phase response. • Cancer cachexia is characterized by lowered muscle Nrk2 expression and NAD+ levels. • Blocking activin receptor 2B ligands rescues muscle NAD+ homeostasis in cachexia. • Blocking activin receptor 2B ligands prevents affected protein synthesis in cachexia. • Serpina3n predicts cachexia and cancer-induced APR independently from muscle atrophy.

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