ReviewMolecular medicine reports2026
Epigenetic orchestration of scar formation: Therapeutic potential of targeting DNA methylation and non‑coding RNAs in cutaneous fibrosis (Review).
Review in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.