PDF(Pubmed)
Abstract：
Knee osteoarthritis (KOA), whose prevalence keeps rising, is still unsolved pathobiological/therapeutical problem. Historically, knee osteoarthritis was thought to be a \"wear and tear\" disease, while recent etiology hypotheses stressed it as a chronic, low-grade inflammatory disease. Inflammasomes mediated by the innate immunity systems have an important role in inflammatory diseases including KOA. A deluge of recent studies focused on the NLRP3 inflammasome with suggestions that its pharmacologic block would hinder degeneration. However, known inflammasomes are numerous and can also trigger IL-1β/IL-18 production and cells\' pyroptotic death. Among them, AIM2 inflammasome is involved in key aspects of various acute and chronic inflammatory diseases. Therefore, while presently leaving out little-studied inflammasomes in KOA, this review focuses on the AIM2 inflammasomes that participate in KOA\'s complex mechanisms in conjunction with the activation of AIM2 inflammasomes in other diseases combined with the current studies on KOA mechanisms. Although human-specific data about it are relatively scant, we stress that only a holistic view including several inflammasomes including AIM2 inflammasome and other potential pathogenetic drivers will lead to successful therapy for knee osteoarthritis.
摘要：
膝骨关节炎（KOA），患病率持续上升，仍然是尚未解决的病理生物学/治疗问题。历史上,膝关节骨关节炎被认为是一种“磨损”疾病，虽然最近的病因学假设强调它是慢性的，低度炎症性疾病。由先天免疫系统介导的炎性体在包括KOA在内的炎性疾病中具有重要作用。最近的大量研究集中在NLRP3炎性体上，并建议其药理阻滞会阻止变性。然而,已知的炎性体数量众多，还可以引发IL-1β/IL-18的产生和细胞焦转性死亡。其中,AIM2炎性体参与各种急性和慢性炎性疾病的关键方面。因此,虽然目前在KOA中忽略了很少研究的炎性体，本文就AIM2炎性体参与KOA的复杂机制以及AIM2炎性体在其他疾病中的激活以及目前对KOA机制的研究作一综述。尽管人类特有的数据相对较少，我们强调,只有包括AIM2炎性体和其他潜在的致病驱动因素在内的多种炎性体的整体观点才能导致膝骨关节炎的成功治疗.
