K
Kouichi Miura
Researcher at Akita University
Publications - 67
Citations - 3700
Kouichi Miura is an academic researcher from Akita University. The author has contributed to research in topics: Internal medicine & Nonalcoholic fatty liver disease. The author has an hindex of 22, co-authored 53 publications receiving 3236 citations. Previous affiliations of Kouichi Miura include Jichi Medical University & University of California, San Diego.
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Journal ArticleDOI
Toll-Like Receptor 9 Promotes Steatohepatitis by Induction of Interleukin-1β in Mice
Kouichi Miura,Kouichi Miura,Yuzo Kodama,Sayaka Inokuchi,Bernd Schnabl,Tomonori Aoyama,Hirohide Ohnishi,Jerrold M. Olefsky,David A. Brenner,Ekihiro Seki +9 more
TL;DR: In a mouse model of NASH, TLR9 signaling induces production of IL-1beta by Kupffer cells, leading to steatosis, inflammation, and fibrosis.
Journal ArticleDOI
Hepatic recruitment of macrophages promotes nonalcoholic steatohepatitis through CCR2
TL;DR: It is concluded that CCR2 and Kupffer cells contribute to the progression of NASH by recruiting bone marrow-derived monocytes.
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Hepatocytes do not undergo epithelial-mesenchymal transition in liver fibrosis in mice.
Kojiro Taura,Kouichi Miura,Keiko Iwaisako,Christoph H. Österreicher,Yuzo Kodama,Melitta Penz-Österreicher,David A. Brenner +6 more
TL;DR: Type I collagen‐producing cells do not originate from hepatocytes, and the concept that hepatocytes in vivo acquire a mesenchymal phenotype through EMT to produce the ECM in liver fibrosis is strongly challenged.
Journal ArticleDOI
Role of gut microbiota and Toll-like receptors in nonalcoholic fatty liver disease
Kouichi Miura,Hirohide Ohnishi +1 more
TL;DR: Gut microbiota and TLRs are targets for NAFLD treatment because they are a source of Toll-like receptor (TLR) ligands, and their compositional change can also increase the amount of TLR ligands delivered to the liver.
Journal ArticleDOI
Disruption of TAK1 in hepatocytes causes hepatic injury, inflammation, fibrosis, and carcinogenesis
Sayaka Inokuchi,Tomonori Aoyama,Kouichi Miura,Christoph H. Österreicher,Yuzo Kodama,Katsumi Miyai,Shizuo Akira,David A. Brenner,Ekihiro Seki +8 more
TL;DR: Hepatocyte-specific deletion of TAK1 in mice resulted in spontaneous hepatocyte death, inflammation, fibrosis, and carcinogenesis that was partially mediated by TNFR signaling, indicating that Tak1 is an essential component for cellular homeostasis in the liver.