ArticleMolecular neurobiology2026
Targeting P2X7R Protects the Retina Against High-Altitude Hypoxia via NLRP3-Mediated Pyroptosis Suppression.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
High-altitude retinopathy (HAR) is a hypoxia-associated retinal disorder whose molecular drivers remain incompletely defined. Here we tested whether purinergic signaling through the P2X7 receptor (P2X7R) amplifies hypoxia-induced retinal damage. In a murine hypobaric hypoxia model, exposure triggered blood-retinal barrier breakdown, retinal edema, and electrophysiological deficits, accompanied by activation of a P2X7R-NLRP3 inflammasome program and induction of pyroptosis-associated effectors. Pharmacological blockade of P2X7R with A740003 (A74) markedly mitigated vascular leakage and structural/functional impairment, while suppressing inflammasome/pyroptosis-related signaling and oxidative stress. In hypoxia-challenged BV2 cell, A74 similarly reduced ROS accumulation, inflammatory activation, and cell injury. Importantly, genetic silencing of P2X7R by siRNA phenocopied the protective effects of A74 by blunting NLRP3/pyroptosis-related responses and dampening pro-inflammatory cytokine output under hypoxia. Together, these results identify P2X7R as a key upstream amplifier of hypoxia-driven inflammatory injury in the retina and nominate P2X7R inhibition as a mechanistically informed intervention strategy for HAR.
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