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Ongoing experimental interest includes its role in neuroendocrine signaling, metabolic regulation, and receptor-mediated cellular pathways

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Mitochondrial dysfunction, characterized by impaired FAO and disrupted quality control mechanisms, has been frequently observed in affected patients ( This metabolic transition is often accompanied by activation of the pentose phosphate pathway (PPP), which may contribute to cellular defense against oxidative stress induced by reactive oxygen species (ROS), as well as a concomitant suppression of gluconeogenesis ( Furthermore, mitochondrial dysfunction is closely implicated in AKI pathogenesis through the activation of inflammatory signaling cascades, which may lead to PTC apoptosis and necrosis ( Although advances in current treatment strategies have improved short-term outcomes, targeted therapies for AKI continue to face significant limitations