ALKBH5-mediated m6A demethylation ameliorates extracellular matrix deposition in cutaneous pathological fibrosis [meRIP-seq]

Hypertrophic scars (HTS) are fibrotic skin disorders characterized by excessive deposition of dermal extracellular matrix (ECM), presenting significant challenges in clinical management despite incomplete understanding of their underlying mechanisms. Using MeRIP-seq and RNA-seq, our study initially revealed the direct regulatory role of ALKBH5 on ECM components in dermal fibroblasts, thereby involving in the pathogenesis of HTS. RNA was obtained from human dermal fibroblasts (HDF) with or without ALKBH5 knockdown. Biological replicates were included.

增生性瘢痕（Hypertrophic scars, HTS）是一类以皮肤真皮细胞外基质（dermal extracellular matrix, ECM）过度沉积为特征的纤维化皮肤疾病，尽管其潜在发病机制尚未完全阐明，但临床管理仍面临显著挑战。本研究采用甲基化RNA免疫沉淀测序（MeRIP-seq）与RNA测序（RNA-seq）技术，首次揭示了ALKBH5对皮肤成纤维细胞中细胞外基质成分的直接调控作用，进而参与增生性瘢痕的致病过程。本研究从经ALKBH5敲低及未敲低的人皮肤成纤维细胞（HDF）中提取RNA，并纳入了生物学重复样本。