Signaling in muscle atrophy and hypertrophy.

By M. Sandri. Physiology, 2008

849 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1bd15d50535c7e24d9c653dbf65f89bc27d085c9

How researchers see this paper

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

In Cardiology and Cardiovascular Medicine

1. S. Schiaffino
2. C. Mammucari
3. Thomas Braun
4. Mathias Gautel
5. M. Sandri

In Cell Biology

1. S. Schiaffino
2. C. Mammucari
3. Thomas Braun
4. Mathias Gautel
5. B. Blaauw
6. M. Komatsu
7. L. Scorrano
8. M. Sandri

In Molecular Biology

1. M. Sandri
2. S. Schiaffino
3. C. Mammucari
4. Lígia C. Gomes
5. Thomas Braun
6. Mathias Gautel
7. B. Blaauw
8. V. Romanello

Citations in the corpus

• Mechanisms regulating skeletal muscle growth and atrophy (2013, background): “5 Sandri M, Lin J, Handschin C, Yang W, Arany ZP, Lecker SH, Goldberg AL & Spiegelman BM (2006) PGC-1a protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene”
• Acute skeletal muscle wasting in critical illness. (2013, background): “ICU length of stay, median (range), d 16 (7-80) 15.”
• Transcriptional mechanisms regulating skeletal muscle differentiation, growth and homeostasis (2011, background): “Signalling through several receptor Tyr kinases activates the phosphoinositide 3-kinase (PI3K)–AKT pathway, a key regulator of muscle mass and metabolism that directly stimulates protein synthesis by activating mammalian target of rapamycin (mTOR) and its downstream target”
• Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models (2011, background): “Various aspects of the role of this pathway in skeletal muscle have been previously discussed [1-3].”
• Mitochondrial fission and remodelling contributes to muscle atrophy (2010, background): “These promoters have been already shown to contain the major regulatory elements for the correct upregulation of these ubiquitin ligases in atrophying muscles (Sandri et al, 2004; Mammucari et al, 2007; Sandri, 2008; Sartori et al, 2009).”
• Autophagy is required to maintain muscle mass. (2009, background): “The two systems are controlled by a transcriptional program that upregulates few critical and rate-limiting enzymes (Sandri, 2008).”
• Regulation of autophagy and the ubiquitin–proteasome system by the FoxO transcriptional network during muscle atrophy (2015, neutral): “Muscles are the largest protein reservoir in the body and serve as a source of amino acids that can be used for energy production by various vital organs (including heart, liver and brain) during catabolic periods, such as in cancer, sepsis, burn injury, heart failure and AIDS 1 .”