PDF(Pubmed)
Abstract：
Atherosclerosis (AS) is the primary pathology behind various cardiovascular diseases and the leading cause of death and disability globally. Recent evidence suggests that AS is a chronic vascular inflammatory disease caused by multiple factors. In this context, the NLRP3 inflammasome, acting as a signal transducer of the immune system, plays a critical role in the onset and progression of AS. The NLRP3 inflammasome is involved in endothelial injury, foam cell formation, and pyroptosis in AS. Therefore, targeting the NLRP3 inflammasome offers a new treatment strategy for AS. This review highlights the latest insights into AS pathogenesis and the pharmacological therapies targeting the NLRP3 inflammasome, focusing on optimal targets for small molecule inhibitors. These insights are valuable for rational drug design and the pharmacological assessment of new targeted NLRP3 inflammasome inhibitors in treating AS.
摘要：
动脉粥样硬化（AS）是各种心血管疾病背后的主要病理和全球死亡和残疾的主要原因。最近的研究表明，AS是一种由多种因素引起的慢性血管炎症性疾病。在这种情况下，NLRP3炎性体,作为免疫系统的信号传感器，在AS的发生和进展中起着至关重要的作用。NLRP3炎性体参与内皮损伤,泡沫细胞的形成，AS中的焦亡。因此,靶向NLRP3炎性体为AS提供了一种新的治疗策略.这篇综述强调了对AS发病机制和靶向NLRP3炎性体的药物治疗的最新见解，专注于小分子抑制剂的最佳靶标。这些见解对于合理的药物设计和新的靶向NLRP3炎性体抑制剂治疗AS的药理学评估是有价值的。
