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Neuroprotective Mechanisms of the ACE2-Angiotensin-(1-7)-Mas Axis in Stroke
Journal article   Peer reviewed

Neuroprotective Mechanisms of the ACE2-Angiotensin-(1-7)-Mas Axis in Stroke

Douglas M. Bennion, Emily Haltigan, Robert W. Regenhardt, U. Muscha Steckelings and Colin Sumners
Current hypertension reports, Vol.17(2), pp.3-3
02/01/2015
DOI: 10.1007/s11906-014-0512-2
PMCID: PMC4378688
PMID: 25620630
url
https://www.ncbi.nlm.nih.gov/pmc/articles/4378688View
Open Access

Abstract

The discovery of beneficial neuroprotective effects of the angiotensin converting enzyme 2-angiotensin-(1-7)Mas axis [ACE2-Ang-(1-7)-Mas] in ischemic and hemorrhagic stroke has spurred interest in a more complete characterization of its mechanisms of action. Here, we summarize findings that describe the protective role of the ACE2Ang-(1-7)-Mas axis in stroke, along with a focused discussion on the potential mechanisms of neuroprotective effects of Ang-(1-7) in stroke. The latter incorporates evidence describing the actions of Ang-(1-7) to counter the deleterious effects of angiotensin II (AngII) via its type 1 receptor, including antiinflammatory, anti-oxidant, vasodilatory, and angiogenic effects, and the role of altered kinase-phosphatase signaling. Interactions of Mas with other receptors, including bradykinin receptors and AngII type 2 receptors are also considered. A more complete understanding of the mechanisms of action of Ang-(1-7) to elicit neuroprotection will serve as an essential step toward research into potential targeted therapeutics in the clinical setting.
Cardiovascular System & Cardiology Life Sciences & Biomedicine Peripheral Vascular Disease Science & Technology

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