Post-stroke inhibition of induced NADPH oxidase type 4 prevents oxidative stress and neurodegeneration.

ABSTRACT: Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human an

SUBMITTER: Kleinschnitz C 

PROVIDER: S-EPMC2943442 | biostudies-literature | 2010 Sep

REPOSITORIES: biostudies-literature