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Acta Physiologica Congress

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Acta Physiologica 2006; Volume 186, Supplement 650
Joint Meeting of The German Society of Physiology and The Federation of European Physiological Societies 2006
3/26/2006-3/29/2006
Ludwig-Maximilians-University, Munich


THE KALLIKREIN-KININ SYSTEM PROMOTES THERAPEUTIC NEOVASCULARIZATION AND HEART PROTECTION
Abstract number: SW2-5

Emanueli1 C

1University of Bristol

Kinins, the biological end-products of the kallikrein-kininogen system, influence many aspects of the cellular function. Our group showed that kinins exert cardiovascular protective effects and promote the recovery of ischaemic limb muscles and the infarcted heart by stimulating angiogenesis and arteriogenesis. Pharmacological and genetic studies indicated that induction of kallikrein and kinin B1 and B2 receptors by ischaemia is functionally relevant in the spontaneous host response which allows for blood flow recovery and tissue healing. Furthermore, the potentiation of the kallikrein-kinin system (KKS) by local gene therapy with human tissue kallikrein (hTK) promoted reparative angiogenesis in the ischaemic limb muscles and the infarcted heart. These effects were mediated by eNOS and Akt-B, but independent of the VEGF-A. In addition, hTK proved useful to prevent apoptosis of vascular cells and skeletal and cardiac myocytes and stimulated the increase in c-kit+/GATA-4+ cardiac progenitor cells (CPCs) in the peri-infarct myocardium. In conclusion, KKS potentiation by hTK or by other strategies able to activate kinin receptors might be applicable to the treatment of coronary artery disease and peripheral ischaemia.

To cite this abstract, please use the following information:
Acta Physiologica 2006; Volume 186, Supplement 650 :SW2-5

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