LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing
Our findings establish lncRNA RMST as a key driver of cutaneous fibrosis through its regulation of Smad3 expression. Targeting the RMST-Smad3 signaling axis therefore represents a promising therapeutic strategy for the treatment and prevention of scarring.
Authors
- Tao Zou (ORCID: https://orcid.org/0000-0002-3667-0060)
- Guokai Dong
- Yang Hai (ORCID: https://orcid.org/0000-0002-2039-5367)
- Chaohang Chen
- Shanshan Li (ORCID: https://orcid.org/0000-0001-6443-958X)
- Xulong Huang
- Zhong Zhou (ORCID: https://orcid.org/0009-0007-1349-8994)
Institutions
- Xuzhou Medical College (CN)
Publication Details
- Journal
- Biochemistry and Biophysics Reports
- Published
- 2025-11-28
- DOI
- https://doi.org/10.1016/j.bbrep.2025.102386
- Primary Topic
- Cancer-related molecular mechanisms research
- Type
- article
- Field-Weighted Citation Impact
- 0.00