LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing.

ABSTRACT:

Background and objective

Scarring presents a significant clinical challenge, imposing both physical and psychological burdens on patients. This drives the need for novel therapeutic strategies. Long non-coding RNAs (lncRNAs) have emerged as pivotal regulators of fibrosis. This study aims to investigate the role of the lncRNA RMST, which we identified as being upregulated during skin wound healing, in the pathogenesis of cutaneous scarring.

Materials and methods

A transcriptomic dataset was analyzed to identify lncRNAs dysregulated during skin wound healing. The function of RMST was assessed using in vivo RMST knockout models in a murine skin wound healing model. Wound tissues were harvested at day 21 post-injury for histological and molecular analysis. Downstream targets of

SUBMITTER: Zhou Z 

PROVIDER: S-EPMC12702190 | biostudies-literature | 2026 Mar

REPOSITORIES: biostudies-literature