Neuroprotective mechanisms of the ACE2-angiotensin-(1-7)-Mas axis in stroke

Curr Hypertens Rep. 2015 Feb;17(2):3. doi: 10.1007/s11906-014-0512-2.

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 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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiotensin I / metabolism*
  • Angiotensin-Converting Enzyme 2
  • Animals
  • Humans
  • Neuroprotective Agents / pharmacology
  • Peptide Fragments / metabolism*
  • Peptidyl-Dipeptidase A / metabolism*
  • Signal Transduction / drug effects
  • Stroke / metabolism*

Substances

  • Neuroprotective Agents
  • Peptide Fragments
  • Angiotensin I
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2
  • angiotensin I (1-7)