摘要
牛皮癣被定义为一种慢性皮肤自身免疫性疾病,其中角质形成细胞的异常增殖和分化被认为是疾病发病的主要原因。环境因素和遗传风险因素之间复杂的相互作用被认为是引发这种疾病的原因。然而,在银屑病的发展过程中,表观遗传调控似乎与外部刺激和遗传异常有关。同卵双胞胎之间牛皮癣患病率的不一致和导致其发病的环境因素已经引起了关于这种疾病发病机制的范式转变。表观遗传失调可能涉及角化细胞分化、t细胞活化和其他可能的细胞异常,导致牛皮癣的发生和持续。表观遗传学的特点是基因转录的可遗传改变而不改变核苷酸,通常在三个水平上考虑,即DNA甲基化,组蛋白修饰和microRNAs。迄今为止,科学证据表明银屑病患者存在异常的DNA甲基化、组蛋白修饰和非编码RNA转录。为了逆转银屑病患者的异常表观遗传变化,已经开发了几种化合物和药物(epi-drugs)来影响参与DNA甲基化或组蛋白乙酰化的主要酶,旨在纠正异常甲基化和乙酰化模式。许多临床试验表明,这类药物在治疗牛皮癣方面具有治疗潜力。在目前的回顾中,我们试图澄清最近的发现,有关银屑病的表观遗传不规则性和讨论未来的挑战。
关键词: 牛皮癣,自身免疫,表观遗传学,DNA甲基化,组蛋白修饰,非编码RNA。
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