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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Sies, Helmut / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred

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IMPACT FACTOR 2017: 3.022

CiteScore 2017: 2.81

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1437-4315
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Volume 387, Issue 6

Issues

The tissue kallikrein-kinin system protects against cardiovascular and renal diseases and ischemic stroke independently of blood pressure reduction

Julie Chao
  • Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Grant Bledsoe
  • Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Hang Yin
  • Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Lee Chao
  • Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2006-06-26 | DOI: https://doi.org/10.1515/BC.2006.085

Abstract

Tissue kallikrein (hK1) cleaves low-molecular-weight kininogen to produce kinin peptide, which binds to kinin receptors and triggers a wide spectrum of biological effects. Tissue kallikrein levels are reduced in humans and in animal models with hypertension, cardiovascular and renal diseases. Transgenic mice or rats over-expressing human tissue kallikrein or kinin B2 receptor are permanently hypotensive, and somatic kallikrein gene delivery reduces blood pressure in several hypertensive rat models. Moreover, kallikrein gene delivery or kallikrein protein infusion can directly improve cardiac, renal and neurological function without blood pressure reduction. Kallikrein has pleiotropic effects in inhibiting apoptosis, inflammation, proliferation, hypertrophy and fibrosis, and promoting angiogenesis and neurogenesis in different experimental animal models. Kallikrein's effects can be blocked by kinin B2 receptor antagonists. Mechanistically, tissue kallikrein/kinin leads to increased nitric oxide levels and Akt activation, and reduced reactive oxygen species formation, TGF-β1 expression, MAPK and nuclear factor-κB activation. Our studies indicate that tissue kallikrein, through the kinin B2 receptor and nitric oxide formation, can protect against oxidative damage in cardiovascular and renal diseases and ischemic stroke. These novel findings suggest that kallikrein/kinin may serve as new drug targets for the prevention and treatment of heart failure, renal disease and stroke in humans.

Keywords: angiogenesis; apoptosis; brain; heart; hypertension; kinin B2 receptor; oxidative stress; tissue kallikrein

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Published Online: 2006-06-26

Published in Print: 2006-06-01


Citation Information: Biological Chemistry, Volume 387, Issue 6, Pages 665–675, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/BC.2006.085.

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