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ACS Applied Nano Materials

ACS Applied Nano Materials

IF: 5.29
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The Mitochondrial-Derived Peptide MOTS-c Alleviates Radiation Pneumonitis via an Nrf2-Dependent Mechanism

Published:17 May 2024 DOI: 10.3390/antiox13050613
Yanli Zhang, Jianfeng Huang, Yaru Zhang, Fengjuan Jiang, Shengpeng Li, Shuai He, Jiaojiao Sun, Dan Chen, Ying Tong, Qingfeng Pang, Yaxian Wu

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.

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Related products
Procduct Name CAS Molecular Formula Supplier Price
MOTS-c 1627580-64-6 C101H152N28O22S2 120 suppliers Inquiry
NF-E2-related factor 2 30 suppliers Inquiry

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