Heart failure-specific cardiac fibroblasts contribute to cardiac dysfunction via the MYC–CXCL1–CXCR2 axis
Jin Komuro(Keio University), Masaki Ieda(University of Tsukuba), Masayuki Kubota(The University of Tokyo), Masamichi Ito(The University of Tokyo), Mai Kimura(Keio University), Seitaro Nomura(The University of Tokyo), Hisayuki Hashimoto(Keio University), Takahiro Nakamura(Kyushu University), Dai Kusumoto(Keio University), Issei Komuro(The University of Tokyo), Toshiomi Katsuki(Keio University), Mikako Katagiri(The University of Tokyo), Keiichi Fukuda(Keio University Hospital), Shintaro Yamada(Tokyo University of Science), Manami Katoh(University of Tokyo Hospital), Yohei Akiba(Keio University), Toshiyuki Ko(The University of Tokyo), Shogo Ito(Kurume University), Kaoruko Komuro(Keio University), Thukaa Kouka(Keio University), Shinsuke Yuasa(Keio University)
Cited by 7
Related Papers
A cross-population atlas of genetic associations for 220 human phenotypes
|Nature Genetics|2021|2.4k
Adult Cardiac Sca-1-positive Cells Differentiate into Beating Cardiomyocytes
|Journal of Biological Chemistry|2004|636
Vascular Cell Senescence
|Circulation Research|2007|527
Cardiac Innervation and Sudden Cardiac Death
|Circulation Research|2015|391
HIF-1α-PDK1 axis-induced active glycolysis plays an essential role in macrophage migratory capacity
|Nature Communications|2016|385