骨格筋神経型一酸化窒素合成酵素により誘起されるCa^<2+>シグナルが筋肥大を促進する(<特集>神経・筋の可塑性とリハビリテーション・スポーツ(69回大会シンポジウムの紹介))

抄録

Skeletal muscle mass is regulated by the balance of protein synthesis and degradation. However, the mechanism by which mechanical load activates protein synthesis remains unknown. We show that neuronal nitric oxide synthase (nNOS) regulates load-induced hypertrophy by activating TRPV1. nNOS was transiently activated by mechanical load. This activation promoted upregulation of mammalian target of rapamycin (mTOR) by increasing intracellular Ca^<2+> concentration. We identified TRPV1 as the target channel of nNOS. Furthermore, administration of the TRPV1 agonist, capsaicin, was sufficient to induce hypertrophy. These results identify nNOS and TRPV1 as the critical mediators that convert mechanical load into intracellular signaling pathway.