ATP, which is released under pathological conditions and is considered a damage-associated molecular pattern (DAMP), activates P2X7 receptors (P2X7Rs), trimeric plasma membrane ion channels selective for small cations. P2X7Rs are partners in NOD-like receptor containing a pyrin (NLRP3) inflammasome activation and promoters of tumor cell growth. P2X7R overstimulation triggers the ATP-dependent opening of a nonselective plasma membrane pore, known as a ‘macropore’, which allows fluxes of large hydrophilic molecules. The pathophysiological functions of P2X7R are thought to be dependent on activation of this conductance pathway, yet its molecular identity is unknown. Recent reports show that P2X7R permeability to organic solutes is an early and intrinsic property of the channel itself. A better understanding of P2X7R-dependent changes in plasma membrane permeability will allow a rationale development of novel anti-inflammatory and anticancer drugs.

在病理条件下释放的ATP被认为是与损伤相关的分子模式（DAMP），可激活P2X7受体（P2X7Rs），对小阳离子具有选择性的三聚质膜离子通道。P2X7Rs是NOD样受体的伴侣，该受体含有吡啶（NLRP3）炎性小体激活和肿瘤细胞生长的启动子。P2X7R过度刺激会触发非选择性质膜孔的ATP依赖性开放，这种孔称为“大孔”，可允许较大的亲水分子通量。P2X7R的病理生理功能被认为依赖于该电导途径的激活，但其分子身份尚不清楚。最近的报道表明，P2X7R对有机溶质的渗透性是通道本身的早期固有特性。