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Licensed Unlicensed Requires Authentication Published by De Gruyter September 13, 2016

Kallikrein(K1)-kinin-kininase (ACE) and end-organ damage in ischemia and diabetes: therapeutic implications

  • Dorinne Desposito , Ludovic Waeckel , Louis Potier , Christine Richer , Ronan Roussel , Nadine Bouby and Francois Alhenc-Gelas EMAIL logo
From the journal Biological Chemistry

Abstract

Genetic and pharmacological studies, clinical and experimental, focused on kallikrein-K1, kinin receptors and ACE/kininase II suggest that kinin release in the settings of ischemia or diabetes reduces organ damage, especially in the heart and kidney. Kinin bioavailability may be a limiting factor for efficacy of current kinin-potentiating drugs, like ACE inhibitors. Primary activation of kinin receptors by prototypic pharmacological agonists, peptidase-resistant, selective B1 or B2, displays therapeutic efficacy in experimental cardiac and peripheral ischemic and diabetic diseases. B1R agonism was especially efficient in diabetic animals and had no unwanted effects. Clinical development of kinin receptor agonists may be warranted.

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Received: 2016-6-10
Accepted: 2016-8-19
Published Online: 2016-9-13
Published in Print: 2016-12-1

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