TFNAs induce autophagy via activation of the nonclassical cGAS–STING signalling pathway to attenuate acute lung injury in mice
This study is the first to demonstrate that TFNAs protect MLE-12 cells against LPS-induced oxidative stress injury via autophagy activated by the nonclassical cGAS-STING signalling pathway. Therefore, TFNAs can attenuate ALI and improve patient prognosis in mice. These findings indicate that the cGAS-STING signalling pathway may be a basic mechanism contributing to various therapeutic immunologic effects. This study demonstrated the value of TFNAs in the treatment of ALI, with potential clinical translational value.
Authors
- Bohan Pan
- Ping Ling (ORCID: https://orcid.org/0000-0002-3229-2365)
- Jiqiu Chen
- Yu Sun (ORCID: https://orcid.org/0000-0003-0863-2769)
- Wei Cui (ORCID: https://orcid.org/0000-0002-2480-8667)
- Jin Zhang (ORCID: https://orcid.org/0000-0001-8738-2301)
- Shihui Zhu (ORCID: https://orcid.org/0009-0008-5127-8148)
- Ying‐Ying Liu (ORCID: https://orcid.org/0000-0001-9185-3380)
- Yang Xiang (ORCID: https://orcid.org/0000-0002-4472-1622)
Institutions
- Shanghai Children's Medical Center (CN)
- Shanghai Changzheng Hospital (CN)
- Burn Institute (US)
Publication Details
- Journal
- BMC Pulmonary Medicine
- Published
- 2025-11-07
- DOI
- https://doi.org/10.1186/s12890-025-03970-w
- Primary Topic
- interferon and immune responses
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China