Mezzaroma Eleonora, Abbate Antonio, Toldo Stefano
Pharmacotherapy and Outcomes Sciences, Virginia Commonwealth University, Richmond, VA, USA.
VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, VA, USA.
Curr Opin Physiol. 2021 Feb;19:105-112. doi: 10.1016/j.cophys.2020.09.013. Epub 2020 Oct 7.
The NACHT, leucine-rich repeat (LRR), and pyrin domain (PYD)-containing protein 3 (NLRP3) inflammasome is a macromolecular structure responsible for the inflammatory response to injury or infection. Several types of heart disease are linked to the activity of the NLRP3 inflammasome and its cytokines, interleukin-1β (IL-1β), and IL-18. Recent pieces of evidence collected from human samples, together with experimental animal models, demonstrate a causative role for the pathogenesis and progression of heart failure (HF). Preclinical research showed that NLRP3 inhibition is a viable strategy to reduce adverse cardiac remodeling and improve left ventricular function in HF. Early phase clinical studies proved to be safe and effective supporting the potential benefit of blocking the NLRP3 inflammasome pathway in patients with HF.
含NACHT、富含亮氨酸重复序列（LRR）和吡啉结构域（PYD）的蛋白3（NLRP3）炎性小体是一种负责对损伤或感染产生炎症反应的大分子结构。几种类型的心脏病与NLRP3炎性小体及其细胞因子白细胞介素-1β（IL-1β）和IL-18的活性有关。从人体样本以及实验动物模型中收集到的最新证据表明，其在心力衰竭（HF）的发病机制和进展中具有因果作用。临床前研究表明，抑制NLRP3是减少HF中不良心脏重塑和改善左心室功能的可行策略。早期临床研究证明该方法安全有效，支持了阻断NLRP3炎性小体途径对HF患者的潜在益处。
