Col23a1 acts as an ECM-resident signal to drive DDR1-p38/ERK-dependent EMT in antimony-induced pulmonary fibrosis
- DOI
- 10.1016/j.cbi.2026.112400
- Published
- 2027-01
- Container
- Chemico-Biological Interactions
- Publisher
- Elsevier BV
- Open access
- unknown
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Cite this work
BibTeX
@article{allodium:10.1016/j.cbi.2026.112400,
title = {Col23a1 acts as an ECM-resident signal to drive DDR1-p38/ERK-dependent EMT in antimony-induced pulmonary fibrosis},
author = {Xin Li and Lirong Chan and Siqi Chen and Ruotong Wu and Zhenzhen Dai and Ling Yang and Yan Zhou and Liling Su},
year = {2027},
journal = {Chemico-Biological Interactions},
doi = {10.1016/j.cbi.2026.112400},
url = {https://doi.org/10.1016/j.cbi.2026.112400}
}RIS
TY - JOUR TI - Col23a1 acts as an ECM-resident signal to drive DDR1-p38/ERK-dependent EMT in antimony-induced pulmonary fibrosis AU - Xin Li AU - Lirong Chan AU - Siqi Chen AU - Ruotong Wu AU - Zhenzhen Dai AU - Ling Yang AU - Yan Zhou AU - Liling Su PY - 2027 JO - Chemico-Biological Interactions DO - 10.1016/j.cbi.2026.112400 UR - https://doi.org/10.1016/j.cbi.2026.112400 ER -
APA
Li, X., Chan, L., Chen, S., Wu, R., Dai, Z., Yang, L., Zhou, Y., & Su, L. (2027). Col23a1 acts as an ECM-resident signal to drive DDR1-p38/ERK-dependent EMT in antimony-induced pulmonary fibrosis. Chemico-Biological Interactions. https://doi.org/10.1016/j.cbi.2026.112400
Source records
- crossref · retrieved 2026-11-10T21:57:25.855Z