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Cardiovascular Research Advance Access originally published online on August 12, 2008
Cardiovascular Research 2008 80(1):7-8; doi:10.1093/cvr/cvn204
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

New pathophysiological function of protein phosphatase 2A?

Joachim Neumann*

Institut für Pharmakologie und Toxikologie, Medizinische Fakultät, Martin-Luther Universität Halle-Wittenberg, Magdeburger Str. 4, Halle 06112, Germany

* Corresponding author. Tel: + 49 345 557 1686; fax: + 49 345 557 18 35. E-mail address: joachim.neumann@medizin.uni-halle.de

This editorial refers to ‘Diastolic dysfunction in alveolar hypoxia: a role for interleukin-18-mediated increase in protein phosphatase 2A’ by Larsen et al.,1 pp. 47–54, this issue.

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In this issue of the Journal, there is an interesting study by Larsen et al.,1 which provides evidence that in pulmonary hypoxia a new mechanism might be operational that explains the deterioration of heart function in primary pulmonary hypertension. The authors chronically exposed mice to 10% oxygen to mimic hypoxia in patients. The authors had noted in previous studies that this degree of pulmonary hypoxia leads to slower cardiac relaxation, . . . [Full Text of this Article]


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Diastolic dysfunction in alveolar hypoxia: a role for interleukin-18-mediated increase in protein phosphatase 2A
Karl-Otto Larsen, Birgitte Lygren, Ivar Sjaastad, Kurt A. Krobert, Kristin Arnkværn, Geir Florholmen, Ann-Kristin Ruud Larsen, Finn Olav Levy, Kjetil Taskén, Ole Henning Skjønsberg, and Geir Christensen
Cardiovasc Res 2008 80: 47-54. [Abstract] [Full Text] [PDF]