Targeting FoxO1/3a, NF-κB, and mTOR signaling attenuates muscle atrophy in sepsis
Donglin Fu, Min Zhou, Yingxiao Zhang, Pan Cheng, Yue Shu, Qian Xiao, Meng Zhang · 2026
Read Targeting FoxO1/3a, NF-κB, and mTOR signaling attenuates muscle atrophy in sepsis by Donglin Fu, Min Zhou, Yingxiao Zhang, Pan Cheng, Yue Shu, Qian Xiao, Meng Zhang (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-13402580.txt.
Description
Donglin Fu and six co-authors trace how sepsis drives skeletal muscle atrophy through three signaling pathways: FoxO1/3a, NF-κB, and mTOR. Sepsis frequently leads to muscle wasting and functional decline, but its molecular mechanisms remained unclear. Their 2026 study pairs a mouse model of sepsis with cultured muscle cells dosed with a bacterial toxin. They track three protein-degrading systems: autophagy, the ubiquitin-proteasome system, and calpain pathways.
All three degradation systems ran hot in sepsis, and muscle function fell. Two signaling pathways that spur the breakdown were upregulated, while mTOR, a growth pathway, was suppressed. Drugs or genetic deletion that blocked key components of these pathways, especially one ubiquitin ligase, mitigated the atrophy and preserved function. The team maps a coordinated drive behind the wasting and names therapeutic targets within it. Human tests would be the next step.
Catalog record
| CREATOR | Donglin Fu, Min Zhou, Yingxiao Zhang, Pan Cheng, Yue Shu, Qian Xiao, Meng Zhang |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 32 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |