Calpain as proposed target for neuroprotective treatment of brain ischemia.
Increasing evidence now suggests that excessive activation of calcium-dependent neutral proteases, calpains, could play a key or contributory role in the pathology of cerebral ischemia. This assumption has been supported in part by the suppressive or neuroprotective effects of calpain inhibitors on post-ischemic damage. Targeting calcium-activated proteolysis could be therefore an alternative strategy for protecting neurons against post-ischemic injury. The data of this review indicate that unregulated activation of calcium-dependent proteolysis plays a significant role in the brain damage that occurs following an ischemic insult and that selective and permanent calpain inhibitors may provide a powerfully effective therapeutic means of limiting neuronal damage.
Zalewska
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Department of Neurochemistry, Medical Research Centre, Polish Academy of Sciences, Warszawa.
D002545:Brain Ischemia / Q000503:physiopathology* / Q000517:prevention & control*; D002154:Calpain / Q000037:antagonists & inhibitors* / Q000502:physiology*; D004151:Dipeptides / Q000627:therapeutic use*; D006801:Humans; D000860:Hypoxia; D009410:Nerve Degeneration
D004151:Dipeptides; C087990:AK 275; D002154:Calpain