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

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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, indicatin

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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