Reversal of cancer cachexia and muscle wasting by ActRIIB antagonism leads to prolonged survival.

By Xiaolan Zhou, Jin Wang, John Lu, Yanping Song, K. S. Kwak, Q. Jiao, R. Rosenfeld, Qing Chen, T. Boone, W. S. Simonet and 3 more. Cell, 2010

911 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/ed3c7e9a982d1d1685da316105ede19d7b816997

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. M. Sandri
2. P. Bonaldo
3. S. Schiaffino
4. C. Mammucari
5. R. Derynck
6. K. Miyazono
7. E. Wagner
8. I. Slaninová

In Physiology

1. S. Schiaffino
2. P. Bonaldo
3. R. Zechner
4. M. Sandri

Citations in the corpus

• TGF-β and the TGF-β Family: Context-Dependent Roles in Cell and Tissue Physiology. (2016, background): “It is worth noting that soluble ActRIIB-Fc, a ligand trap for myostatin, activin, and GDF-11, prevents muscle wasting and reverses loss of skeletal muscle and cardiac atrophy in tumor-bearing mice with cachexia (Zhou et al. 2010).”
• Cellular and molecular mechanisms of muscle atrophy (2013, background): “A recent study showed that inhibition of myostatin by soluble ActRIIB prevents and fully reverses skeletal muscle loss and atrophy of the heart in tumor-bearing animals (Zhou et al., 2010).”
• A switch from white to brown fat increases energy expenditure in cancer-associated cachexia. (2014, background): “At the molecular level, changes described in skeletal muscle of cachectic mice (Zhou et al., 2010), such as increased nuclear staining of phospho-SMAD2, increased expression of the cell-cycle inhibitor p21, the proapoptotic gene Bax, and the proinflammatory cytokine interleukin-6 (IL-6), were…”
• Growth Differentiation Factor 11 is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy (2013, neutral): “Thus, we speculate that the reported ActRIIB antagonist effects on myocardium (Zhou et al., 2010) may be due to inhibition of GDF11 signaling and independent of effects on myostatin.”
• Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models (2011, background): “In adult skeletal muscle, muscle hypertrophy can be induced and muscle wasting prevented by blocking myostatin either via postdevelopmental myostatin gene knockout, or with follistatin (a myostatin antagonist) or anti-myostatin antibodies or a soluble ActRIIB decoy receptor (see [19,20] and referenc”