Neuroprotective Mechanisms of the ACE2–Angiotensin-(1-7)–Mas Axis in Stroke
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  • 作者:Douglas M. Bennion ; Emily Haltigan ; Robert W. Regenhardt…
  • 关键词:Angiotensin converting enzyme 2 ; Angiotensin ; (1 ; 7) ; Mas ; Angiotensin type 1 receptor ; Angiotensin type 2 receptor ; Renin ; angiotensin system ; Stroke ; Neuroprotection ; Neuron ; Microglia ; Ischemia ; Intracerebral hemorrhage ; Inflammation
  • 刊名:Current Hypertension Reports
  • 出版年:2015
  • 出版时间:February 2015
  • 年:2015
  • 卷:17
  • 期:2
  • 全文大小:1,164 KB
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  • 作者单位:Douglas M. Bennion (1)
    Emily Haltigan (1)
    Robert W. Regenhardt (1)
    U. Muscha Steckelings (2)
    Colin Sumners (1)

    1. Department of Physiology and Functional Genomics & McKnight Brain Institute, University of Florida, 1600 SW Archer Road, PO Box 100274, Gainesville, FL, 32610-0274, USA
    2. Department of Cardiovascular and Renal Research, University of Southern Denmark, J.B. Winsl?ws Vej 21 3, 5000, Odense C, Denmark
  • 刊物主题:Internal Medicine; Cardiology; Metabolic Diseases; Nephrology; Primary Care Medicine; General Practice / Family Medicine;
  • 出版者:Springer US
  • ISSN:1534-3111
文摘
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 ACE2–Ang-(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 anti-inflammatory, 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.

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