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Table 2 Mechanisms and clinical value of DNA methylation in keloid

From: Epigenetic modification mechanisms involved in keloid: current status and prospect

DNA methylation Expression Mechanism Clinical value Ref
HOXA9/HOXA10 Hypermethylation DNA methylation altered wound healing in keloid fibroblasts Strategies to treat or prevent keloids [50]
CDC2L1 Hypermethylation DNA methylation of the CDC2L1 gene promoter resulted in decreased fibroblast apoptosis, thus promoting the development of keloids The potential therapeutic value in the process of wound healing for preventing keloid development [14]
SFRP1 Hypermethylation The SFRP1 promoter methylation significantly promoted the signaling activity of Wnt/β-catenin and the mRNA and protein expression of β-catenin and α-SMA in keloid fibroblasts A therapeutic target for keloid treatment [52]
POMC Hypermethylation POMC gene promoter methylation would not account for the development of hypopigmentation in keloid N/A [53]
  1. DNA methylation without base sequence alteration is considered as the most common and highly dynamic epigenetic modification. The potential reversibility of the DNA methylation pattern may be beneficial for therapeutic choices