Phosphodiesterase 9A controls nitric-oxide-independent cGMP and hypertrophic heart disease

Dong I. Lee, Guangshuo Zhu, Takashi Sasaki, Gun-Sik Cho, Nazha Hamdani, Ronald Holewinski, Su-Hyun Jo, Thomas Danner, Manling Zhang, Peter P. Rainer, Djahida Bedja, Jonathan A. Kirk, Mark J. Ranek, Wolfgang R. Dostmann, Chulan Kwon, Kenneth B. Margulies, Jennifer E. Van Eyk, Walter J. Paulus, Eiki Takimoto and David A. Kass ()
Additional contact information
Dong I. Lee: The Johns Hopkins Medical Institutions
Guangshuo Zhu: The Johns Hopkins Medical Institutions
Takashi Sasaki: Advanced Medical Research Laboratories, Mitsubishi Tanabe Pharma Corporation, Yokohama, Kanagawa 227-0033, Japan
Gun-Sik Cho: The Johns Hopkins Medical Institutions
Nazha Hamdani: Institute for Cardiovascular Research, VU University Medical Center, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
Ronald Holewinski: The Johns Hopkins Medical Institutions
Su-Hyun Jo: Institute of Bioscience and Biotechnology, BK21 plus Graduate Program, Kangwon National University College of Medicine
Thomas Danner: The Johns Hopkins Medical Institutions
Manling Zhang: The Johns Hopkins Medical Institutions
Peter P. Rainer: The Johns Hopkins Medical Institutions
Djahida Bedja: The Johns Hopkins Medical Institutions
Jonathan A. Kirk: The Johns Hopkins Medical Institutions
Mark J. Ranek: The Johns Hopkins Medical Institutions
Wolfgang R. Dostmann: University of Vermont
Chulan Kwon: The Johns Hopkins Medical Institutions
Kenneth B. Margulies: Cardiovascular Institute, Perelman School of Medicine, University of Pennsylvania
Jennifer E. Van Eyk: The Johns Hopkins Medical Institutions
Walter J. Paulus: Institute for Cardiovascular Research, VU University Medical Center, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
Eiki Takimoto: The Johns Hopkins Medical Institutions
David A. Kass: The Johns Hopkins Medical Institutions

Nature, 2015, vol. 519, issue 7544, 472-476

Abstract: The inhibition, in mice, of the phosphodiesterase PDE9A, which specifically regulates natriuretic-peptide-coupled cGMP signalling, is independent of nitric oxide and is upregulated in failing human hearts, and can reverse pre-established stress-induced heart disease.

Date: 2015
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DOI: 10.1038/nature14332

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