Cutaneous fibrosis is sustained by epigenetic 'memory' rather than chronic inflammation.DNA hypermethylation, repressive histone marks and non-coding RNA networks lock dermal fibroblasts into a collagen-secretory state that can persist years after wounding.Single-cell methylomes have identified DNA methyltransferase (DNMT)3B as the key epigenetic writer driving anti-fibrotic gene silencing, whereas N6-methyladenosine-modified long non-coding RNAs and reinforce these loops by tethering methylation machinery to chromatin.Local delivery of DNMT inhibitors, microRNA-29 mimics or antisense oligonucleotides via dissolvable microneedles, metal-organic framework patches or exosome arrays reproducibly reduces scar volume by 25-55% in pre-clinical models without systemic exposure of therapeutic agents.The present review integrates multi-omic mechanistic data with emerging device platforms to chart a precision roadmap for converting scar-forming repair into scar-sparing regeneration. Contents1. Introduction 2. Epigenetic toolbox and emerging technologies 3. DNA methylation drivers of cutaneous fibrosis 4. ncRNA networks in scar pathogenesis 5. Histone modifications and chromatin accessibility in scar fibroblasts 6. Crosstalk between DNA methylation and ncRNAs 7. From proof-of-concept to scar-sparing intervention 8. Future directions and outstanding questions 9. Conclusions
Li et al. (Fri,) studied this question.
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