The world’s number one cause of death is cardiovascular diseases. The pathogenesis of different disease entities in the cardiovascular disease spectrum is complicated and multifactorial. Inflammation in these complicated etiologies serves as a key position and is a significant cause of atherosclerosis, which contributes to the underlying pathology. Therefore, therapeutic targeting of inflammatory pathways in patients with cardiovascular diseases such as atherosclerosis enhances cardiovascular results. Inflammasomes are intracellular protein complexes engaged in atherosclerosis pathogenesis and activated by multiple danger signals. Emerging proof has revealed that Nod-like receptor protein 3 (NLRP3) inflammasome, which regulates caspase-1 activation and later pro-interleukin processing, triggers inflammatory reactions in the vascular wall and leads to atherosclerotic plaque formation. Inflammasome-mediated signaling interference could decrease inflammation and mitigate illness severity. In this section, we provide an overview of the present literature on the underlying mechanisms leading to the activation of NLRP3 inflammasome and the role of NLRP3 inflammasome in the progression of atherogenesis and highlight the possibility of therapeutic interventions due to mechanisms involved in the of inhibition of NLRP3 activation.

世界第一大死因是心血管疾病。心血管疾病谱中不同疾病实体的发病机制是复杂且多因素的。这些复杂病因中的炎症是一个关键位置，是动脉粥样硬化的重要原因，这有助于潜在的病理学。因此，针对心血管疾病（如动脉粥样硬化）患者的炎症通路的治疗可提高心血管结果。炎症小体是参与动脉粥样硬化发病机制并被多种危险信号激活的细胞内蛋白质复合物。新出现的证据表明，Nod 样受体蛋白 3 (NLRP3) 炎症小体可调节 caspase-1 的激活和随后的白介素前体加工，引发血管壁的炎症反应并导致动脉粥样硬化斑块的形成。炎症小体介导的信号干扰可以减少炎症并减轻疾病的严重程度。在本节中，我们概述了目前关于导致 NLRP3 炎性体激活的潜在机制以及 NLRP3 炎性体在动脉粥样硬化进展中的作用的文献，并强调了由于参与抑制的机制而进行治疗干预的可能性。 NLRP3 激活。