Zobrazeno 1 - 10
of 40
pro vyhledávání: '"Eri Iwai-Kanai"'
Autor:
Atsushi Hoshino, Shunta Taminishi, Yoshito Minami, Satoaki Matoba, Ryota Urata, Tomohiro Hino, Takashi Nakagawa, Yohei Fushimura, Eri Iwai-Kanai, Satoru Furukawa
Publikováno v:
Biochemical and Biophysical Research Communications. 585:191-195
Impairment of pancreatic β cells is a principal driver of the development of diabetes. Restoring normal insulin release from the β cells depends on the ATP produced by the intracellular mitochondria. In maintaining mitochondrial function, the tumor
Autor:
Eri Iwai-Kanai, Daiki Shimomura, Akira Kondo, Hiroyuki Ito, Shuji Matsuo, Yoshikazu Yamamoto, Yoshihisa Nakagawa, Noriko Hatanaka, Misato Nakatani, Hirokazu Kondo
Publikováno v:
The Journal of Applied Laboratory Medicine. 5:1216-1227
BackgroundProtein induced by vitamin K absence-II (PIVKA-II) is produced by the liver during hepatoma and upon warfarin administration. Those patients have disturbed protein synthesis and glycosylation in the liver. This decreases the number of γ-ca
Publikováno v:
Journal of Clinical Biochemistry and Nutrition
Thioredoxin is a low molecular weight (approximately 12 kDa) redox protein, and protects against harmful stimuli such as oxidative stress. Smoking evokes oxidative stress, among other biological responses. The clinical relevance of thioredoxin in smo
Autor:
Ryoetsu Yamanaka, Sakiko Honda, Eri Iwai-Kanai, Atsushi Hoshino, Daichi Hato, Satoaki Matoba, Yohei Fushimura, Ryota Urata, Yoshito Minami, Kuniyoshi Fukai
Publikováno v:
American journal of physiology. Heart and circulatory physiology. 319(5)
Yamanaka R, Hoshino A, Fukai K, Urata R, Minami Y, Honda S, Fushimura Y, Hato D, Iwai-Kanai E, Matoba S. TIGAR reduces smooth muscle cell autophagy to prevent pulmonary hypertension. Am J Physiol Heart Circ Physiol 319: H1087-H1096, 2020. First publi
Autor:
Motoki Uchihashi, Shuhei Tateishi, Satoaki Matoba, Kazunori Ono, Makoto Ariyoshi, Kuniyoshi Fukai, Satoshi Kaimoto, Yoshifumi Okawa, Eri Iwai-Kanai, Atsushi Hoshino
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 312:H305-H313
Failing heart loses its metabolic flexibility, relying increasingly on glucose as its preferential substrate and decreasing fatty acid oxidation (FAO). Peroxisome proliferator-activated receptor α (PPAR-α) is a key regulator of this substrate shift
Autor:
Tomoya Kitani, Eri Iwai-Kanai, Ryoetsu Yamanaka, Ryota Urata, Yoshifumi Okawa, Tomohiro Hino, Satoaki Matoba, Yoshito Minami, Shunta Taminishi, Daichi Hato, Nobuichiro Yagi, Sakiko Honda, Yohei Fushimura, Atsushi Hoshino, Ayumi Matsuki, Shyo Hashimoto, toshiyuki nishiji
Publikováno v:
Circulation Research. 125
Background: Although metabolic alterations were observed in heart failure (HF), only recently have the mechanisms underlying these changes been identified. Tumor suppressor p53 responds to metabolic changes thorough several mechanisms. One of the p53
Autor:
Satoaki Matoba, Yohei Fushimura, Yusuke Higuchi, Takehiro Ogata, Ryoetsu Yamanaka, Atsushi Hoshino, Kazunori Ono, Satoshi Kaimoto, Shuhei Tateishi, Yoshifumi Okawa, Kuniyoshi Fukai, Daichi Hato, Sakiko Honda, Makoto Ariyoshi, Eri Iwai-Kanai, Motoki Uchihashi
Publikováno v:
Circulation: Heart Failure. 10
Background Energy starvation and the shift of energy substrate from fatty acids to glucose is the hallmark of metabolic remodeling during heart failure progression. However, ketone body metabolism in the failing heart has not been fully investigated.
Autor:
Makoto Ariyoshi, Yohei Fushimura, Daichi Hato, Ryoetsu Yamanaka, Atsushi Hoshino, Masashi Mita, Naotada Ishihara, Satoaki Matoba, Eri Iwai-Kanai, Yuichiro Mita, Yurika Miyoshi, Maiko Nakane, Sakiko Honda, Syuhei Tateishi, Motoki Uchihashi, Hiroshi Homma, Masumi Katane, Kuniyoshi Fukai, Yoshifumi Okawa, Kazunori Ono, Kenji Hamase, Satoshi Kaimoto
Publikováno v:
Scientific Reports
D-Amino acids are enantiomers of L-amino acids and have recently been recognized as biomarkers and bioactive substances in mammals, including humans. In the present study, we investigated functions of the novel mammalian mitochondrial protein 9030617
Autor:
Tomomi Ueyama, Maki Katamura, Satoaki Matoba, Mikihiko Nakaoka, Eri Iwai-Kanai, Masaki Kimata, Atsushi Hoshino, Koji Ikeda, Hiroaki Matsubara, Yoshifumi Okawa, Makoto Ariyoshi, Hideo Nakamura, Mitsuhiko Okigaki, Yuichiro Mita
Publikováno v:
Journal of Molecular and Cellular Cardiology. 52:175-184
Inhibition of tumor suppressor p53 is cardioprotective against ischemic injury and provides resistance to subsequent cardiac remodeling. We investigated p53-mediated expansion of ischemic damage with a focus on mitochondrial integrity in association
Autor:
Yoshihiro Yui, Ken-ichirou Watanabe, Yoshimi Hiraumi, Tatsutoshi Nakahata, Motonobu Watanabe, Hiroaki Matsubara, Souichi Adachi, Shinya Toyokuni, Yasuhiro Mizushima, Yuri Kamitsuji, Shiro Baba, Hiroshi Matsubara, Eri Iwai-Kanai
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 296:H823-H832
Although granulocyte colony-stimulating factor (G-CSF) reportedly plays a cardioprotective role in several models of cardiac injury, clinical use of this drug in cardiac patients has been controversial. Here, we tested, in vivo and in vitro, the effe