Table 2 Molecular mechanisms driving skeletal muscle atrophy during cachexia, evidence derived from human studies are italicized
From: Understanding cachexia as a cancer metabolism syndrome
Skeletal muscle wasting | ||
|---|---|---|
UPR | Upregulation of the ubiquitin-proteasome pathway in cancer model | Baracos et al.60 |
Proteasome and NF-kB inhibitors prevent experimental cancer cachexia | Chacon-Cabrera et al.65 | |
UPR activation is required for muscle atrophy | Bodine et al.59 | |
Authophagy | It is induced in the skeletal muscle of cancer patients | Op den Kamp et al.70 Tardif et al.71 Boyer-Guittaut et al.72 |
Promotes muscle wasting during cachexia | Penna et al.68 | |
ActRIIB | Decoy receptor reverses muscle wasting | Zhou et al.50 |
Cachectic patients present increased circulating levels of ActRIIB ligand, activin | Loumaye et al.49 | |
Myostatin (ActRIIB ligand) knock-out prevents experimental cachexia | Gallot et al.48 | |
Lipid wasting | ||
Lipolysis | Adipose Triglyceride Lipase inhibition prevents muscle wasting in experimental cachexia. | Das and Hoefler117 |
Cachectic cancer patients present increased lipolytic activity | ||
