ArticleCellular and molecular neurobiology2026
Nitric Oxide Donor Alleviates Cardiac Arrest Induced Blood Brain Barrier Injury by Inhibiting HMGB1-ATG5 Mediated Endothelial Autophagy.
Article in Cellular and 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
Cardiac arrest (CA) and subsequent cardiopulmonary resuscitation (CPR) often cause severe neurological deficits due to ischemia–reperfusion (I/R) injury, marked by systemic inflammation, blood–brain barrier (BBB) dysfunction, and excessive autophagy. JS-K, a nitric oxide-releasing prodrug, has shown cytoprotective effects, but its role in CA-induced brain injury remains unclear. Here, we investigated the therapeutic potential of JS-K in a mouse CA/CPR model and an in vitro oxygen–glucose deprivation/reoxygenation (OGD/R) model. JS-K treatment improved neurological outcomes, preserved BBB function, and prolonged survival. Mechanistically, JS-K preserved tight junction proteins and improved BBB function and suppressed endothelial autophagy in vivo and in vitro. Further analyses revealed that HMGB1, after nuclear-cytoplasmic translocation, interacted with ATG5, inducing excessive autophagy and BBB injury. JS-K inhibited HMGB1 translocation, reduced HMGB1-ATG5 interaction, and consequently mitigated autophagy-driven BBB dysfunction. Notably, ATG5 silencing failed to enhance JS-K’s protective effects, supporting that JS-K acts at least in part through the HMGB1-ATG5 axis. These findings identify JS-K as a promising therapeutic agent that targets HMGB1-mediated autophagy to protect BBB function after cardiac arrest.
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