Signalling pathways that mediate skeletal muscle hypertrophy and atrophy

By D. Glass. Nature Cell Biology, 2003

717 citations recorded by the source corpus.

How researchers see this paper

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

Interleukin-6 is an essential regulator of satellite cell-mediated skeletal muscle hypertrophy. (2008, background): “The activation of the AKT/mTOR pathway and its downstream targets p70 S6K and 4E-BP1 by controlling net protein content is a crucial regulator of skeletal muscle hypertrophic growth (Bodine et al., 2001; Glass, 2003, 2005).”
Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression (2004, background): “Beyond helping us understand these important responses, this analysis may identify therapeutic targets for retarding the atrophy process (26).”
The Molecular Bases of Training Adaptation (2007, background): “There are three isoforms of the serine / threonine AKT family, two of which (AKT1 and 2) are primarily expressed in skeletal muscle (Glass 2003; Nader 2005).”
The role of FoxO in the regulation of metabolism (2008, background): “There are two muscle-specific ubiquitin ligases: atrogin-1 (MAFbx) and MuRF-1 (muscle ring finger-1) (Glass, 2003).”
IGF-I stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin ligases, atrogin-1 and MuRF1. (2004, background): “IGF-I also activates the MEK-ERK pathway, and glucocorticoid induction of Ub mRNA is transcriptionally regulated by MEK1 (30), although the potential importance of this pathway in skeletal muscle hypertrophy is uncertain (11).”