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

Author

Listed:
  • 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)

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.

Suggested Citation

  • Masanori Sano & Tohru Minamino & Haruhiro Toko & Hideyuki Miyauchi & Masayuki Orimo & Yingjie Qin & Hiroshi Akazawa & Kaoru Tateno & Yosuke Kayama & Mutsuo Harada & Ippei Shimizu & Takayuki Asahara & , 2007. "p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload," Nature, Nature, vol. 446(7134), pages 444-448, March.
    • Handle: RePEc:nat:nature:v:446:y:2007:i:7134:d:10.1038_nature05602
    DOI: 10.1038/nature05602
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    Cited by:

    1. Muhammad Imran & Muhammad Nadeem & Muhammad Asif Khan & Sheraz Ahmed & Ali Imran & Rai Muhammad Amir & Muhammad Umair Arshad & Syed Amir Gilani & Farhan Saeed & Abdur Rauf & Zaffar Mehmood & Shaista K, 2017. "Curcumin and its allied analogues: epigenetic and health perspectives - a review," Czech Journal of Food Sciences, Czech Academy of Agricultural Sciences, vol. 35(4), pages 285-310.
    2. Toshiyuki Ko & Seitaro Nomura & Shintaro Yamada & Kanna Fujita & Takanori Fujita & Masahiro Satoh & Chio Oka & Manami Katoh & Masamichi Ito & Mikako Katagiri & Tatsuro Sassa & Bo Zhang & Satoshi Hatsu, 2022. "Cardiac fibroblasts regulate the development of heart failure via Htra3-TGF-β-IGFBP7 axis," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    3. Fabian Peisker & Maurice Halder & James Nagai & Susanne Ziegler & Nadine Kaesler & Konrad Hoeft & Ronghui Li & Eric M. J. Bindels & Christoph Kuppe & Julia Moellmann & Michael Lehrke & Christian Stopp, 2022. "Mapping the cardiac vascular niche in heart failure," Nature Communications, Nature, vol. 13(1), pages 1-20, December.

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