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Beyond mechanistic models, multiple studies of ischemia-reperfusion injury, acute kidney injury, delayed graft dysfunction, and the transition from acute kidney injury to chronic kidney disease now support the presence of ferroptotic spread along renal tubular epithelia in intact disease settings, with evidence of trigger-wave dynamics, extracellular vesicle-mediated signaling, oxidized lipid mediators, and transcriptional or metabolic reprogramming circuits
(PubMed) van Zuuren EJ, Albusta AY, Fedorowicz Z, Carter B, Pijl H
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