Inflammasomes are a class of cytosolic protein complexes. They act as cytosolic innate immune signal receptors to sense pathogens and initiate inflammatory responses under physiological and pathological conditions. The NLR-family pyrin domain-containing protein 3 (NLRP3) inflammasome is the most characteristic multimeric protein complex. Its activation triggers the cleavage of pro-interleukin (IL)-1β and pro-IL-18, which are mediated by caspase-1, and secretes mature forms of these mediators from cells to promote the further inflammatory process and oxidative stress. Simultaneously, cells undergo pro-inflammatory programmed cell death, termed pyroptosis. The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage. Vascular endothelium at the site of inflammation is actively involved in the regulation of inflammation progression with important implications for cardiovascular homeostasis as a dynamically adaptable interface. Endothelial dysfunction is a hallmark and predictor for cardiovascular ailments or adverse cardiovascular events, such as coronary artery disease, diabetes mellitus, hypertension, and hypercholesterolemia. The loss of proper endothelial function may lead to tissue swelling, chronic inflammation, and the formation of thrombi. As such, elimination of endothelial cell inflammation or activation is of clinical relevance. In this review, we provided a comprehensive perspective on the pivotal role of NLRP3 inflammasome activation in aggravating oxidative stress and endothelial dysfunction and the possible underlying mechanisms. Furthermore, we highlighted the contribution of noncoding RNAs to NLRP3 inflammasome activation-associated endothelial dysfunction, and outlined potential clinical drugs targeting NLRP3 inflammasome involved in endothelial dysfunction. Collectively, this summary provides recent developments and perspectives on how NLRP3 inflammasome interferes with endothelial dysfunction and the potential research value of NLRP3 inflammasome as a potential mediator of endothelial dysfunction.

炎症小体是一类胞质蛋白复合物。它们作为细胞质先天免疫信号受体来感知病原体并在生理和病理条件下启动炎症反应。 NLR 家族包含热蛋白结构域的蛋白 3 (NLRP3) 炎性体是最具特征性的多聚蛋白复合物。它的激活会触发由 caspase-1 介导的白细胞介素原 (IL)-1β 和 IL-18 前体的裂解，并从细胞中分泌这些介质的成熟形式，以促进进一步的炎症过程和氧化应激。同时，细胞经历促炎性程序性细胞死亡，称为细胞焦亡。激活NLRP3炎症小体的危险信号非常广泛，尤其是活性氧（ROS），它作为激活NLRP3炎症小体的中间触发因素，加剧随后的炎症级联反应和细胞损伤。炎症部位的血管内皮积极参与炎症进展的调节，作为动态适应性界面，对心血管稳态具有重要意义。内皮功能障碍是心血管疾病或不良心血管事件（例如冠状动脉疾病、糖尿病、高血压和高胆固醇血症）的标志和预测因素。适当内皮功能的丧失可能导致组织肿胀、慢性炎症和血栓形成。因此，消除内皮细胞炎症或活化具有临床意义。在这篇综述中，我们对 NLRP3 炎症小体激活在加重氧化应激和内皮功能障碍中的关键作用以及可能的潜在机制提供了全面的视角。 此外，我们强调了非编码RNA对NLRP3炎症小体激活相关的内皮功能障碍的贡献，并概述了针对参与内皮功能障碍的NLRP3炎症小体的潜在临床药物。总的来说，本总结提供了 NLRP3 炎症小体如何干扰内皮功能障碍的最新进展和观点，以及 NLRP3 炎症小体作为内皮功能障碍的潜在介质的潜在研究价值。