S
Seitaro Nomura
Researcher at University of Tokyo
Publications - 60
Citations - 1516
Seitaro Nomura is an academic researcher from University of Tokyo. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 14, co-authored 42 publications receiving 827 citations. Previous affiliations of Seitaro Nomura include Jichi Medical University.
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Journal ArticleDOI
Dysbiosis and compositional alterations with aging in the gut microbiota of patients with heart failure
Takehiro Kamo,Hiroshi Akazawa,Wataru Suda,Wataru Suda,Akiko Saga-Kamo,Yu Shimizu,Hiroki Yagi,Qing Liu,Seitaro Nomura,Atsuhiko T. Naito,Norifumi Takeda,Mutsuo Harada,Haruhiro Toko,Hidetoshi Kumagai,Yuichi Ikeda,Eiki Takimoto,Jun-ichi Suzuki,Kenya Honda,Hidetoshi Morita,Masahira Hattori,Masahira Hattori,Issei Komuro +21 more
TL;DR: It is suggested that patients with HF harbor significantly altered gut microbiota, which varies further according to age, and new concept of heart-gut axis has a great potential for breakthroughs in the development of novel diagnostic and therapeutic approach for HF.
Journal ArticleDOI
Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure
Seitaro Nomura,Masahiro Satoh,Takanori Fujita,Tomoaki Higo,Tomokazu Sumida,Toshiyuki Ko,Toshihiro Yamaguchi,Takashige Tobita,Atsuhiko T. Naito,Masamichi Ito,Kanna Fujita,Mutsuo Harada,Haruhiro Toko,Yoshio Kobayashi,Kaoru Ito,Eiki Takimoto,Hiroshi Akazawa,Hiroyuki Morita,Hiroyuki Aburatani,Issei Komuro +19 more
TL;DR: The authors identify the gene programs encoding the morphological and functional characteristics of cardiomyocytes during the transition from early hypertrophy to heart failure via single-cell transcriptomics, establishing a key role for p53 signalling.
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Population-specific and trans-ancestry genome-wide analyses identify distinct and shared genetic risk loci for coronary artery disease.
Satoshi Koyama,Kaoru Ito,Chikashi Terao,Masato Akiyama,Momoko Horikoshi,Yukihide Momozawa,Hiroshi Matsunaga,Hirotaka Ieki,Kouichi Ozaki,Yoshihiro Onouchi,Atsushi Takahashi,Seitaro Nomura,Hiroyuki Morita,Hiroshi Akazawa,Changhoon Kim,Jeong-Sun Seo,Koichiro Higasa,Koichiro Higasa,Motoki Iwasaki,Taiki Yamaji,Norie Sawada,Shoichiro Tsugane,Teruhide Koyama,Hiroaki Ikezaki,Naoyuki Takashima,Naoyuki Takashima,Keitaro Tanaka,Kokichi Arisawa,Kiyonori Kuriki,Mariko Naito,Mariko Naito,Kenji Wakai,Shinichiro Suna,Yasuhiko Sakata,Hiroshi Sato,Masatsugu Hori,Yasushi Sakata,Koichi Matsuda,Yoshinori Murakami,Hiroyuki Aburatani,Michiaki Kubo,Fumihiko Matsuda,Yoichiro Kamatani,Yoichiro Kamatani,Issei Komuro +44 more
TL;DR: A large-scale genome-wide association study of 168,228 individuals of Japanese ancestry with genotype imputation with genotypes imputation detected eight new susceptibility loci and Japanese-specific rare variants contributing to disease severity and increased cardiovascular mortality, and a trans-ancestry meta-analysis found 35 additional new loci.
Journal ArticleDOI
Promotion of CHIP-Mediated p53 Degradation Protects the Heart From Ischemic Injury
Atsuhiko T. Naito,Sho Okada,Tohru Minamino,Koji Iwanaga,Mei-Lan Liu,Tomokazu Sumida,Seitaro Nomura,Naruhiko Sahara,Tatsuya Mizoroki,Akihiko Takashima,Hiroshi Akazawa,Toshio Nagai,Ichiro Shiojima,Issei Komuro +13 more
TL;DR: In this paper, the authors investigated the molecular mechanisms of p53 accumulation in the heart after myocardial infarction and tested whether anti-p53 approach would be effective against myocardious infarctions.
Journal ArticleDOI
DNA single-strand break-induced DNA damage response causes heart failure
Tomoaki Higo,Atsuhiko T. Naito,Tomokazu Sumida,Masato Shibamoto,Katsuki Okada,Seitaro Nomura,Akito Nakagawa,Toshihiro Yamaguchi,Taku Sakai,Akihito Hashimoto,Yuki Kuramoto,Masamichi Ito,Shungo Hikoso,Hiroshi Akazawa,Hiroshi Akazawa,Jong-Kook Lee,Ichiro Shiojima,Peter J. McKinnon,Yasushi Sakata,Issei Komuro,Issei Komuro +20 more
TL;DR: In this article, the role of DNA single-strand break (SSB) in the pathogenesis of pressure overload-induced heart failure was investigated in mice lacking XRCC1, an essential protein for SSB repair.