Shin'ichi Takeda and colleagues show that loading of muscle results in nitric oxide creation and its conversion to peroxynitrite. The latter molecule then activates TRPV1 in the muscle, leading to increased cytoplasmic concentrations of calcium and activation of mTOR and, thus, muscle hypertrophy. They could replicate these effects without overload by treating mice with a TRPV1 agonist, suggesting a possible therapy for muscle wasting.
- Naoki Ito
- Urs T Ruegg
- Shin'ichi Takeda
