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- Title
The Mitochondrial-Derived Peptide MOTS-c Alleviates Radiation Pneumonitis via an Nrf2-Dependent Mechanism.
- Authors
Zhang, Yanli; Huang, Jianfeng; Zhang, Yaru; Jiang, Fengjuan; Li, Shengpeng; He, Shuai; Sun, Jiaojiao; Chen, Dan; Tong, Ying; Pang, Qingfeng; Wu, Yaxian
- Abstract
Radiation pneumonitis (RP) is a prevalent and fatal complication of thoracic radiotherapy due to the lack of effective treatment options. RP primarily arises from mitochondrial injury in lung epithelial cells. The mitochondrial-derived peptide MOTS-c has demonstrated protective effects against various diseases by mitigating mitochondrial injury. C57BL/6 mice were exposed to 20 Gy of lung irradiation (IR) and received daily intraperitoneal injections of MOTS-c for 2 weeks. MOTS-c significantly ameliorated lung tissue damage, inflammation, and oxidative stress caused by radiation. Meanwhile, MOTS-c reversed the apoptosis and mitochondrial damage of alveolar epithelial cells in RP mice. Furthermore, MOTS-c significantly inhibited oxidative stress and mitochondrial damage in MLE-12 cells and primary mouse lung epithelial cells. Mechanistically, MOTS-c increased the nuclear factor erythroid 2-related factor (Nrf2) level and promoted its nuclear translocation. Notably, Nrf2 deficiency abolished the protective function of MOTS-c in mice with RP. In conclusion, MOTS-c alleviates RP by protecting mitochondrial function through an Nrf2-dependent mechanism, indicating that MOTS-c may be a novel potential protective agent against RP.
- Subjects
RADIATION pneumonitis; LUNGS; PEPTIDES; EPITHELIAL cells; INTRAPERITONEAL injections; RADIOTHERAPY complications
- Publication
Antioxidants, 2024, Vol 13, Issue 5, p613
- ISSN
2076-3921
- Publication type
Article
- DOI
10.3390/antiox13050613