A study in human patients with second-degree burns demonstrated that the miR-506-3p was downregulated in burn tissues compared to normal tissues, and its expression increased following treatment with an artificial skin membrane, correlating with improved wound healing, reduced fibrosis markers (Col1A1, α-SMA), and decreased inflammatory cytokines (TNF-α, IL-6, IL-8) [Li et al. DOI:10.1002/jcla.24564]. A separate review of human studies identified the miR-506-3p as downregulated in <24h post-burn in third-degree burn skin and in heat-treated human skin fibroblast cell lines versus controls [Siu et al. DOI:10.1111/wrr.13100]. A review of human, rat, and mouse models further indicates that the miR-506-3p is downregulated in burned tissues and heat-damaged fibroblasts, where it inhibits fibroblast proliferation and induces autophagy by targeting Beclin-1 and TGF-β1, affecting extracellular matrix synthesis [Wang et al. DOI:10.1007/s00438-024-02183-w].