ArticleBiochemistry and biophysics reports2026
LncRNA RMST knockout inhibits fibrosis by down-regulating Smad3 during mouse skin wound healing.
Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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 RMST were predicted through bioinformatic analysis and validated using quantitative RT-PCR and Western blot. Finally, a rescue experiment was performed by overexpressing Smad3 in the context of RMST knockout to confirm the functional hierarchy. Results: RMST knockout significantly suppressed fibrotic progression and inflammatory activity at day 21 post-injury, demonstrated by reduced collagen deposition and lower levels of key inflammatory mediators. Bioinformatic and experimental analyses identified Smad3 as a key downstream target. RMST knockout directly reduced both Smad3 mRNA and protein levels, indicating a direct regulatory mechanism acting at the expression level. Crucially, the anti-fibrotic effects of RMST knockout were effectively reversed upon Smad3 overexpression, confirming that Smad3 acts functionally downstream of RMST. Conclusion: 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.
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