Nature Communications (Jun 2022)
Cardiac fibroblasts regulate the development of heart failure via Htra3-TGF-β-IGFBP7 axis
- 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 Hatsuse,
- Takanobu Yamada,
- Mutsuo Harada,
- Haruhiro Toko,
- Eisuke Amiya,
- Masaru Hatano,
- Osamu Kinoshita,
- Kan Nawata,
- Hiroyuki Abe,
- Tetsuo Ushiku,
- Minoru Ono,
- Masashi Ikeuchi,
- Hiroyuki Morita,
- Hiroyuki Aburatani,
- Issei Komuro
Affiliations
- Toshiyuki Ko
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Seitaro Nomura
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Shintaro Yamada
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Kanna Fujita
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Takanori Fujita
- Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo
- Masahiro Satoh
- Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo
- Chio Oka
- Laboratory of Functional Genomics and Medicine, Nara Institute of Science and Technology
- Manami Katoh
- Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo
- Masamichi Ito
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Mikako Katagiri
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Tatsuro Sassa
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Bo Zhang
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Satoshi Hatsuse
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Takanobu Yamada
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Mutsuo Harada
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Haruhiro Toko
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Eisuke Amiya
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Masaru Hatano
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Osamu Kinoshita
- Department of Cardiac Surgery, Graduate School of Medicine, The University of Tokyo
- Kan Nawata
- Department of Cardiovascular Surgery, St. Marianna University School of Medicine
- Hiroyuki Abe
- Department of Pathology, Graduate School of Medicine, The University of Tokyo
- Tetsuo Ushiku
- Department of Pathology, Graduate School of Medicine, The University of Tokyo
- Minoru Ono
- Department of Cardiac Surgery, Graduate School of Medicine, The University of Tokyo
- Masashi Ikeuchi
- Department of Biodesign, Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University
- Hiroyuki Morita
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- Hiroyuki Aburatani
- Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo
- Issei Komuro
- Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
- DOI
- https://doi.org/10.1038/s41467-022-30630-y
- Journal volume & issue
-
Vol. 13,
no. 1
pp. 1 – 17
Abstract
Cardiac fibrosis is a hallmark of heart failure. Here the authors use single-cell RNA-sequencing, spatial transcriptomics, and genetic manipulations, to show that Htra3 regulates cardiac fibrosis by keeping fibroblasts quiescent and by degrading TGF-beta.
