表观遗传学
小RNA
疾病
背景(考古学)
DNA甲基化
骨关节炎
组蛋白
生物信息学
生物
发病机制
机制(生物学)
医学
遗传学
免疫学
基因
基因表达
病理
古生物学
替代医学
哲学
认识论
作者
Anwar Fathollahi,Saeed Aslani,Ahmadreza Jamshidi,Mahdi Mahmoudi
摘要
Abstract Osteoarthritis (OA) is the most common type of arthritis and no longer is considered as an absolute consequence of joint mechanical use (wear and tear); rather recent data demonstrate the pivotal role of inflammatory mediators in the development and progression of this disease. This multifactorial disease results from several environmental and inherited factors. Genetic cannot solely explain all the contribution share of inheritance and, this way, it is speculated that epigenetics can play a role, too. Moreover, environmental factors can induce local epigenetic changes. The epigenetic contribution to OA pathogenesis occurs at all of its levels, DNA methylation, histone modification, microRNA, and long noncoding RNA. In fact, during early phases of OA pathogenesis, environmental factors employ epigenetic mechanisms to provide a positive feedback for the OA‐related pathogenic mechanisms and pathways with an ultimate outcome of a well‐established clinical OA. These epigenetic changes stay during clinical disease and prevent the body natural healing and regenerative processes to work properly, resulting in an incurable disease condition. In this review article, we aimed to have an overview on the studies performed with regard to understanding the role of epigenetics in the etiopathogenesis of OA and highlighted the importance of such kind of regulatory mechanisms within this context.
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