Journal
BIOMEDICINES
Volume 9, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines9111667
Keywords
ischemic stroke; angiotensin converting enzyme-2; MasR; therapy
Categories
Funding
- National Institute of Health National Institutes of Health [NIGMS 5 P20 GM121307-02]
- Department of Neurology, LSUHSC-Shreveport
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Ischemic stroke is the leading cause of neurologically based morbidity and mortality, and current treatments are limited to two classes of FDA-approved drugs with a narrow time-window for administration. There is a desperate need for new stroke therapies to suppress the deleterious effects of ischemic injury.
Ischemic stroke remains the leading cause of neurologically based morbidity and mortality. Current stroke treatment is limited to two classes of FDA-approved drugs: thrombolytic agents (tissue plasminogen activator (tPA)) and antithrombotic agents (aspirin and heparin), which have a narrow time-window (<4.5 h) for administration after onset of stroke symptoms. While thrombolytic agents restore perfusion, they carry serious risks for hemorrhage, and do not influence damage responses during reperfusion. Consequently, stroke therapies that can suppress deleterious effects of ischemic injury are desperately needed. Angiotensin converting enzyme-2 (ACE2) has been recently suggested to beneficially influence experimental stroke outcomes by converting the vasoconstrictor Ang II into the vasodilator Ang 1-7. In this review, we extensively discuss the protective functions of ACE2-Ang (1-7)-MasR axis of renin angiotensin system (RAS) in ischemic stroke.
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