http://nro.sagepub.com/content/19/2/129.abstract?etoc
Abstract
In ischemic stroke, apoptosis persists for
days to weeks after the onset of an ischemic event. Cysteine-ASPartic
proteASEs
(caspases) are key mediators of apoptosis and
neurodegeneration in stroke. The impact of caspase activity is not
restricted
to neuronal death, as caspases can exacerbate
inflammation and alter glial function. Thus, caspases are logical
therapeutic
targets for this disease, but they have never been
clinically evaluated due to a paucity of ideal drug candidates. Recent
developments in caspase inhibition and drug
delivery offer novel neuroprotective strategies for stroke, which are
deliberated
in this review.
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