| First Author | Yuasa K | Year | 2018 |
| Journal | Sci Rep | Volume | 8 |
| Issue | 1 | Pages | 9037 |
| PubMed ID | 29899565 | Mgi Jnum | J:263213 |
| Mgi Id | MGI:6162841 | Doi | 10.1038/s41598-018-26632-w |
| Citation | Yuasa K, et al. (2018) Targeted ablation of p38alpha MAPK suppresses denervation-induced muscle atrophy. Sci Rep 8(1):9037 |
| abstractText | The loss of skeletal muscle mass is a major cause of falls and fractures in the elderly, leading to compromised independence and a decrease in the quality of life. However, only a few therapeutic interventions leading to marginal clinical benefits in patients with this condition are currently available. Therefore, the demand to further understand the pathology of muscle atrophy and establish a treatment modality for patients with muscle atrophy is significant. p38alpha mitogen-activated protein kinase (p38alpha MAPK) is a ubiquitous signaling molecule that is implicated in various cellular functions, including cell proliferation, differentiation, and senescence. In the present study, we generated a mutant line in which p38alpha MAPK is specifically abrogated in muscle tissues. Compared with the control mice, these mutant mice are significantly resistant to denervation-induced muscle atrophy, suggesting that p38alpha MAPK positively regulates muscle atrophy. We also identified CAMK2B as a potential downstream target of p38alpha MAPK and found that the pharmacological inhibition of CAMK2B activity suppresses denervation-induced muscle atrophy. Altogether, our findings identify p38alpha MAPK as a novel regulator of muscle atrophy and suggest that the suppression of intracellular signaling mediated by p38alpha MAPK serves as a potential target for the treatment of muscle atrophy. |
