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Experimental study reveals that inhibiting SGK1 reduces cerebral injury and neurological deficits after cardiac arrest, highlighting a potential neuroprotective therapeutic target.
Upregulation of SGK1 exacerbates brain injury during cerebral ischemia. Inhibition of SGK1 affords neuroprotection against cardiac arrest-induced hypoperfusion, neuroinflammation, neuronal cell death, and neurological deficits.
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Lee et al. (2020) studied this question.
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