An intense, stereotyped inflammatory response occurs in response to ischaemic and non-ischaemic injury to the myocardium. The NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome is a finely regulated macromolecular protein complex that senses the injury and triggers and amplifies the inflammatory response by activation of caspase 1; cleavage of pro-inflammatory cytokines, such as pro-IL-1β and pro-IL-18, to their mature forms; and induction of inflammatory cell death (pyroptosis). Inhibitors of the NLRP3 inflammasome and blockers of IL-1β and IL-18 activity have been shown to reduce injury to the myocardium and pericardium, favour resolution of the inflammation and preserve cardiac function. In this Review, we discuss the components of the NLRP3 inflammasome and how it is formed and activated in various ischaemic and non-ischaemic cardiac pathologies (acute myocardial infarction, cardiac dysfunction and remodelling, atherothrombosis, myocarditis and pericarditis, cardiotoxicity and cardiac sarcoidosis). We also summarize current preclinical and clinical evidence from studies of agents that target the NLRP3 inflammasome and related cytokines.

强烈的、刻板的炎症反应发生在心肌缺血性和非缺血性损伤的反应中。包含 NACHT、LRR 和 PYD 结构域的蛋白 3 （NLRP3） 炎性小体是一种精细调节的大分子蛋白复合物，可感知损伤并通过激活 caspase 1 触发和放大炎症反应;促炎细胞因子（如 pro-IL-1β 和 pro-IL-18）裂解成成熟形式;和诱导炎性细胞死亡 （焦亡）。NLRP3 炎性小体抑制剂以及 IL-1β 和 IL-18 活性阻滞剂已被证明可以减少心肌和心包的损伤，有利于炎症的消退并保留心脏功能。在这篇综述中，我们讨论了 NLRP3 炎性小体的成分以及它是如何在各种缺血性和非缺血性心脏病（急性心肌梗死、心功能不全和重塑、动脉粥样硬化血栓形成、心肌炎和心包炎、心脏毒性和心脏结节病）中形成和激活的。我们还总结了针对 NLRP3 炎性小体和相关细胞因子的药物研究的当前临床前和临床证据。