系统性自身免疫性疾病中的m6A RNA甲基化——基于表观遗传学治疗的新靶点?
m6A RNA Methylation in Systemic Autoimmune Diseases-A New Target for Epigenetic-Based Therapy?
作者信息
Wardowska Anna
机构信息
Department of Embryology, Medical University of Gdansk, 80-210 Gdansk, Poland.
出版信息
Pharmaceuticals (Basel). 2021 Mar 5;14(3):218. doi: 10.3390/ph14030218.
The general background of autoimmune diseases is a combination of genetic, epigenetic and environmental factors, that lead to defective immune reactions. This erroneous immune cell activation results in an excessive production of autoantibodies and prolonged inflammation. During recent years epigenetic mechanisms have been extensively studied as potential culprits of autoreactivity. Alike DNA and proteins, also RNA molecules are subjected to an extensive repertoire of chemical modifications. N6-methyladenosine is the most prevalent form of internal mRNA modification in eukaryotic cells and attracts increasing attention due to its contribution to human health and disease. Even though m6A is confirmed as an essential player in immune response, little is known about its role in autoimmunity. Only few data have been published up to date in the field of RNA methylome. Moreover, only selected autoimmune diseases have been studied in respect of m6A role in their pathogenesis. In this review, I attempt to present all available research data regarding m6A alterations in autoimmune disorders and appraise its role as a potential target for epigenetic-based therapies.
自身免疫性疾病的一般背景是遗传、表观遗传和环境因素的综合作用,这些因素会导致免疫反应缺陷。这种错误的免疫细胞激活会导致自身抗体过度产生和炎症持续。近年来,表观遗传机制作为自身反应性的潜在罪魁祸首受到了广泛研究。与DNA和蛋白质一样,RNA分子也会经历广泛的化学修饰。N6-甲基腺苷是真核细胞中最普遍的内部mRNA修饰形式,因其对人类健康和疾病的影响而受到越来越多的关注。尽管m6A被确认为免疫反应中的重要参与者,但其在自身免疫中的作用却知之甚少。到目前为止,RNA甲基化组领域只有很少的数据发表。此外,关于m6A在其发病机制中的作用,仅对少数自身免疫性疾病进行了研究。在这篇综述中,我试图展示所有关于自身免疫性疾病中m6A改变的现有研究数据,并评估其作为基于表观遗传治疗的潜在靶点的作用。