Nature Communications (Sep 2016)
ANGPTL2 activity in cardiac pathologies accelerates heart failure by perturbing cardiac function and energy metabolism
- Zhe Tian,
- Keishi Miyata,
- Tsuyoshi Kadomatsu,
- Haruki Horiguchi,
- Hiroyuki Fukushima,
- Shugo Tohyama,
- Yoshihiro Ujihara,
- Takahiro Okumura,
- Satoshi Yamaguchi,
- Jiabin Zhao,
- Motoyoshi Endo,
- Jun Morinaga,
- Michio Sato,
- Taichi Sugizaki,
- Shunshun Zhu,
- Kazutoyo Terada,
- Hisashi Sakaguchi,
- Yoshihiro Komohara,
- Motohiro Takeya,
- Naoki Takeda,
- Kimi Araki,
- Ichiro Manabe,
- Keiichi Fukuda,
- Kinya Otsu,
- Jun Wada,
- Toyoaki Murohara,
- Satoshi Mohri,
- Jun K. Yamashita,
- Motoaki Sano,
- Yuichi Oike
Affiliations
- Zhe Tian
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Keishi Miyata
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Tsuyoshi Kadomatsu
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Haruki Horiguchi
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Hiroyuki Fukushima
- Department of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University
- Shugo Tohyama
- Department of Cardiovascular Medicine, School of Medicine, Keio University
- Yoshihiro Ujihara
- First Department of Physiology, Kawasaki Medical School
- Takahiro Okumura
- Department of Cardiology, Nagoya University Graduate school of Medicine
- Satoshi Yamaguchi
- Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
- Jiabin Zhao
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Motoyoshi Endo
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Jun Morinaga
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Michio Sato
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Taichi Sugizaki
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Shunshun Zhu
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Kazutoyo Terada
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- Hisashi Sakaguchi
- Department of Cardiovascular Surgery, Graduate School of Medical Sciences, Kumamoto University
- Yoshihiro Komohara
- Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University
- Motohiro Takeya
- Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University
- Naoki Takeda
- Institute of Resource Developmental and Analysis, Kumamoto University
- Kimi Araki
- Institute of Resource Developmental and Analysis, Kumamoto University
- Ichiro Manabe
- Department of Aging Research, Graduate School of Medicine, Chiba University
- Keiichi Fukuda
- Department of Cardiovascular Medicine, School of Medicine, Keio University
- Kinya Otsu
- Cardiovascular Division, King’s College London British Heart Foundation Centre of Research Excellence
- Jun Wada
- Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
- Toyoaki Murohara
- Department of Cardiology, Nagoya University Graduate school of Medicine
- Satoshi Mohri
- First Department of Physiology, Kawasaki Medical School
- Jun K. Yamashita
- Department of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University
- Motoaki Sano
- Department of Cardiovascular Medicine, School of Medicine, Keio University
- Yuichi Oike
- Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
- DOI
- https://doi.org/10.1038/ncomms13016
- Journal volume & issue
-
Vol. 7,
no. 1
pp. 1 – 19
Abstract
Heart responds to increased workload by enlarging cardiomyocytes to preserve function, but in pathologies hypertrophy leads to heart failure. Here the authors show that ANGPTL2 activity in the heart is critical for determining beneficial vs. pathological hypertrophy via its effect on AKT-SERCA2a signaling and myocardial energy.
