SPP1 induces idiopathic pulmonary fibrosis and NSCLC progression via the PI3K/Akt/mTOR pathway
Our findings suggest that SPP1 functions as a molecule promoting both fibrosis and tumorigenesis, positioning it as a prospective therapeutic target for managing the co-occurrence of IPF and NSCLC.
Authors
- Bingqing Yue
- Fei Gao (ORCID: https://orcid.org/0000-0002-4086-2575)
- Xiucheng Yang (ORCID: https://orcid.org/0000-0002-0038-8928)
- Dian Xiong (ORCID: https://orcid.org/0000-0002-8905-9046)
- Jingyu Chen (ORCID: https://orcid.org/0000-0002-2127-1788)
- Wei Dong (ORCID: https://orcid.org/0000-0002-8107-3900)
- Jingbo Shao
- Juan Chen (ORCID: https://orcid.org/0000-0002-6099-4671)
- Jin Zhao (ORCID: https://orcid.org/0009-0009-8428-1703)
- Man Huang (ORCID: https://orcid.org/0000-0003-1358-2567)
Institutions
- Nanchang University (CN)
- Second Affiliated Hospital of Nanchang University (CN)
- Second Affiliated Hospital of Zhejiang University (CN)
- Zhejiang University (CN)
Publication Details
- Journal
- Respiratory Research
- Published
- 2024-10-05
- DOI
- https://doi.org/10.1186/s12931-024-02989-7
- Citations
- 41
- Primary Topic
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Type
- article
- Field-Weighted Citation Impact
- 17.18
Funders
- National Natural Science Foundation of China