Overload-mediated skeletal muscle hypertrophy is not impaired by loss of myofiber STAT3

Joaquin Perez-Schindler, Mary C. Esparza, James McKendry, Leigh Breen, Andrew Philp, Simon Schenk

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)
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Although the signal pathways mediating muscle protein synthesis and degradation are well characterized, the transcriptional processes modulating skeletal muscle mass and adaptive growth are poorly understood. Recently, studies in mouse models of muscle wasting or acutely exercised human muscle have suggested a potential role for the transcription factor, signal transducer and activator of transcription 3 (STAT3), in adaptive growth. Hence, in the present study we sought to define the contribution of STAT3 to skeletal muscle adaptive growth. In contrast to previous work, two different resistance exercise protocols did not change STAT3 phosphorylation in human skeletal muscle. To directly address the role of STAT3 in load-induced (i.e. adaptive) growth, we studied the anabolic effects of 14 days of synergist ablation (SA) in skeletal muscle-specific STAT3 knockout (mKO) mice and their floxed, wild type (WT) littermates. Plantaris muscle weight and fibre area in the non-operated leg (Control; CON) was comparable between genotypes. As expected, SA significantly increased plantaris weight, muscle fibre cross sectional area and anabolic signalling in WT mice, although interestingly, this induction was not impaired in STAT3 mKO mice. Collectively, these data demonstrate that STAT3 is not required for overload-mediated hypertrophy in mouse skeletal muscle.
Original languageEnglish
Pages (from-to)C257-C261
JournalAJP: Cell Physiology
Issue number3
Publication statusPublished - 28 Jun 2017


  • hypertrophy
  • resistance exercise
  • STAT3
  • skeletal muscle


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