Abstract：
Atopic dermatitis, commonly referred to as atopic eczema, is a persistent inflammatory skin disorder that predominantly manifests in children but may endure into adulthood. Its clinical management poses challenges due to the absence of a definitive cure, and its prevalence varies across ethnicities, genders, and geographic locations. The epigenetic landscape of AD includes changes in DNA methylation, changes in histone acetylation and methylation, and regulation by non-coding RNAs. These changes affect inflammatory and immune mechanisms, and research has identified AD-specific variations in DNA methylation, particularly in the affected epidermis. Histone modifications, including acetylation, have been associated with the disruption of skin barrier function in AD, suggesting the potential therapeutic benefit of histone deacetylase inhibitors such as belinostat. Furthermore, non-coding RNAs, particularly microRNAs and long non-coding RNAs (lncRNAs), have been implicated in modulating various cellular processes central to AD pathogenesis. Therapeutic implications in AD include the potential use of DNA methylation inhibitors and histone deacetylase inhibitors to correct aberrant methylation patterns and modulate gene expression related to immune responses and skin barrier functions. Additionally, the emerging role of lncRNAs suggests the possibility of using small interfering RNAs or antisense oligonucleotides to inhibit lncRNAs and adjust their regulatory impact on gene expression. In conclusion, the importance of epigenetic elements in AD is becoming increasingly clear as studies highlight the contribution of DNA methylation, histone modifications and, control by non-coding RNAs to the onset and progression of the disease. Understanding these epigenetic changes provides valuable insights for developing targeted therapeutic strategies.
摘要：
特应性皮炎,通常被称为特应性湿疹，是一种持续的炎症性皮肤病，主要表现在儿童身上，但可能持续到成年。由于缺乏明确的治疗方法，其临床管理带来了挑战，其患病率因种族而异，性别,和地理位置。AD的表观遗传景观包括DNA甲基化的变化，组蛋白乙酰化和甲基化的变化，和非编码RNA的调控。这些变化影响炎症和免疫机制，研究已经确定了DNA甲基化的AD特异性变异，特别是在受影响的表皮。组蛋白修改,包括乙酰化，与AD中皮肤屏障功能的破坏有关，提示组蛋白去乙酰化酶抑制剂如belinostat的潜在治疗益处。此外，非编码RNA，特别是microRNA和长链非编码RNA（lncRNAs），与调节AD发病机理的各种细胞过程有关。AD的治疗意义包括DNA甲基化抑制剂和组蛋白脱乙酰酶抑制剂的潜在用途，以纠正异常的甲基化模式并调节与免疫反应和皮肤屏障功能相关的基因表达。此外,lncRNAs的新作用提示了使用小干扰RNAs或反义寡核苷酸抑制lncRNAs并调节其对基因表达的调控作用的可能性。总之,随着研究强调DNA甲基化的贡献，表观遗传元件在AD中的重要性变得越来越明显，组蛋白修饰和，由非编码RNA控制疾病的发作和进展。了解这些表观遗传变化为制定有针对性的治疗策略提供了有价值的见解。
