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<p>Keloid is a trauma-induced fibroproliferative condition characterized by excessive extracellular matrix (ECM) deposition and aberrant keloid fibroblast activation, leading to physical, psychological, functional, and cosmetic impairments. This study investigates DNA methylation alterations at Long Interspersed Nuclear Element-1 (LINE-1) and Alu repetitive elements in keloid tissues compared to normal skin tissues. Methylation levels and patterns were analyzed in keloid (<i>n</i> = 38) and normal skin tissues (<i>n</i> = 32). The results revealed significantly lower LINE-1 (<i>P</i> &lt; 0.0001) and Alu (<i>P</i> = 0.0147) methylation levels in keloids, with hypomethylation inversely correlated with chronological age. Younger individuals exhibited higher methylation levels compared to older individuals. These findings offer critical insights into the epigenetic mechanisms underlying keloid formation and progression, providing a foundation for developing epigenetic-based therapeutic strategies.</p>

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Methylation of LINE-1 and Alu repetitive sequence in keloid

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月30日

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  • Piyawan Prabsattru,
  • Tanchanok Nakbua,
  • Suthida Sengphairogh,
  • Nakarin Kitkumthorn,
  • Jiraroch Meevassana

摘要

Keloid is a trauma-induced fibroproliferative condition characterized by excessive extracellular matrix (ECM) deposition and aberrant keloid fibroblast activation, leading to physical, psychological, functional, and cosmetic impairments. This study investigates DNA methylation alterations at Long Interspersed Nuclear Element-1 (LINE-1) and Alu repetitive elements in keloid tissues compared to normal skin tissues. Methylation levels and patterns were analyzed in keloid (n = 38) and normal skin tissues (n = 32). The results revealed significantly lower LINE-1 (P < 0.0001) and Alu (P = 0.0147) methylation levels in keloids, with hypomethylation inversely correlated with chronological age. Younger individuals exhibited higher methylation levels compared to older individuals. These findings offer critical insights into the epigenetic mechanisms underlying keloid formation and progression, providing a foundation for developing epigenetic-based therapeutic strategies.