p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload

Masanori Sano, Tohru Minamino, Haruhiro Toko, Hideyuki Miyauchi, Masayuki Orimo, Yingjie Qin, Hiroshi Akazawa, Kaoru Tateno, Yosuke Kayama, Mutsuo Harada, Ippei Shimizu, Takayuki Asahara, Hirofumi Hamada, Shuhei Tomita, Jeffrey D. Molkentin, Yunzeng Zou and Issei Komuro ()
Additional contact information
Masanori Sano: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Tohru Minamino: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Haruhiro Toko: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Hideyuki Miyauchi: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Masayuki Orimo: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Yingjie Qin: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Hiroshi Akazawa: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Kaoru Tateno: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Yosuke Kayama: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Mutsuo Harada: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Ippei Shimizu: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
Takayuki Asahara: Stem Cell Translational Research, Kobe Institute of Biomedical Research and Innovation/RIKEN Center for Developmental Biology, 2-2 Minatojima-Minamimachi, Chuo-ku, Kobe 650-0047, Japan
Hirofumi Hamada: Sapporo Medical University, S1 W17, Chuo-ku, Sapporo 060-8556, Japan
Shuhei Tomita: Institute for Genome Research, University of Tokushima, 3-18-15 Kuramoto, Tokushima 770-8503, Japan
Jeffrey D. Molkentin: Children’s Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229-3039, USA
Yunzeng Zou: Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, 180 Feng Lin Road, Shanghai 200032, China
Issei Komuro: Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan

Nature, 2007, vol. 446, issue 7134, 444-448

Abstract: Heading off heart failure Cardiac enlargement, or hypertrophy, is a physiological response to increased workload and helps to maintain cardiac function. If the condition is prolonged, however, it can develop into heart failure. New insight into how that transition occurs has been obtained in a study of a mouse model of cardiac hypertrophy. As the animal's heart enlarges, new blood vessels develop to support it. But after about two weeks, the tumour suppressor protein p53 accumulates in heart cells, angiogenesis is blocked and the mice suffer cardiac failure. Targeting this process by inhibiting p53 or by promoting angiogenesis may be a means of preventing the transition from cardiac hypertrophy to heart failure.

Date: 2007
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DOI: 10.1038/nature05602

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