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Preclinical findings revealed that AMPK the brain from seizure-induced neuronal death through induction of Bcl-2modifying factor (Bmf) normally interacts with the cytoskeleton, but upon certain cellular stresses, such as loss of extracellular matrix adhesion or energy crisis, Bmf relocalizes to mitochondria, where it can promote Bax activation and mitochondrial dysfunction (Moran et al

2010;(3):CD001942

This strategy is likely to be associated with a reduction of kidney disease progression at the long term

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