Edificio LAIB 4ª Planta, Instituto Murciano de Investigación Biosanitaria (IMIB-Arrixaca), Hospital Clínico Universitario Virgen de la Arrixaca, Carretera Buenavista s/n. 30120 El Palmar, Murcia, Spain.
Biochem Pharmacol. 2021 May;187:114385. doi: 10.1016/j.bcp.2020.114385. Epub 2020 Dec 20.
Adenosine triphosphate (ATP) is a molecule that on one hand plays a central role in cellular energetics and which on the other is a ubiquitous signaling molecule when released into the extracellular media. Extracellular ATP accumulates in inflammatory environments where it acts as a damage-associated molecular pattern and activates the purinergic P2X receptor 7 (P2X7) in immune cells. P2X7 receptor activation induces the formation of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3 (NLRP3) inflammasome and the activation of the inflammatory caspase-1. Caspase-1 causes an inflammatory type of cell death called pyroptosis through the release of pro-inflammatory cytokines and intracellular content. Consequently, intense research efforts have been devoted to the design of novel anti-inflammatory therapies, focusing in particular on the P2X7 receptor and the NLRP3 pathway and the introduction of new blocking molecules in early phase clinical trials.
三磷酸腺苷（ATP）一方面在细胞能量学中起着核心作用，另一方面当它被释放到细胞外介质中时，它是一种无处不在的信号分子。细胞外 ATP 在炎症环境中积累，在炎症环境中，它作为一种损伤相关分子模式，激活免疫细胞中的嘌呤能 P2X 受体 7（P2X7）。P2X7 受体的激活诱导核苷酸结合域、富含亮氨酸的家族、含有吡喃结构域 3（NLRP3）炎症小体的形成以及炎症性半胱天冬酶-1 的激活。通过释放促炎细胞因子和细胞内内容物，炎症性半胱天冬酶-1 引起一种称为细胞焦亡的炎症性细胞死亡。因此，人们投入了大量的研究努力来设计新型抗炎疗法，特别是针对 P2X7 受体和 NLRP3 途径，并在早期临床试验中引入新的阻断分子。
