Laboratory Research 19SP02 'Chronic Pathologies: From Genome to Management', Department of Respiratory Diseases, Tunis El Manar University.
Department of Respiratory Diseases, Pavillon B. Abderrahman Mami Hospital, Tunis, Tunisia.
Curr Opin Rheumatol. 2024 Jan 1;36(1):9-15. doi: 10.1097/BOR.0000000000000962. Epub 2023 Aug 13.
Vasculitis are a group of heterogeneous conditions characterized by chronic inflammation of blood vessels, leading to tissue destruction and organ failure. Vasculitis is an inflammatory process in which immune effector cells infiltrate blood vessels and surrounding tissues. The involvement of inflammasomes seems to occur during inflammatory processes.
Studies have emphasized that genetic susceptibility is an important aspect of the pathogenesis of vasculitis. The innate immune system is a major contributor to these inflammatory diseases, suggesting that the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome plays a key role. NLRP3 activation causes the assembly of a large multiprotein and leads to the secretion of bioactive interleukin (IL)-1β and IL-18 as well as the induction of inflammatory cell death, termed pyroptosis. Accumulating evidence confirms the involvement of this cascade in sterile inflammatory diseases and other vascular diseases.
In this review, we will summarize the current state of knowledge regarding the role of NLRP3 inflammasome in vascular diseases, and discuss the potential of the NLRP3 inflammasome as a therapeutic target.
血管炎是一组异质性疾病，其特征为血管慢性炎症，导致组织破坏和器官衰竭。血管炎是一种免疫效应细胞浸润血管及周围组织的炎症过程。炎性小体的参与似乎发生在炎症过程中。
研究强调遗传易感性是血管炎发病机制的一个重要方面。先天免疫系统是这些炎症性疾病的主要贡献者，这表明 NOD 样受体家族含 pyrin 结构域 3（NLRP3）炎性小体发挥关键作用。NLRP3 激活导致大型多蛋白的组装，并导致生物活性白细胞介素 (IL)-1β和 IL-18 的分泌以及炎症细胞死亡，称为细胞焦亡。越来越多的证据证实了这一级联反应在无菌性炎症性疾病和其他血管疾病中的参与。
在这篇综述中，我们将总结 NLRP3 炎性小体在血管疾病中的作用的最新知识，并讨论 NLRP3 炎性小体作为治疗靶点的潜力。
