Cardiac dopamine D1 receptor triggers ventricular arrhythmia in chronic heart failure

Toshihiro Yamaguchi, Tomokazu S. Sumida, Seitaro Nomura, Masahiro Satoh, Tomoaki Higo, Masamichi Ito, Toshiyuki Ko, Kanna Fujita, Mary E. Sweet, Atsushi Sanbe, Kenji Yoshimi, Ichiro Manabe, Toshikuni Sasaoka, Matthew R. G. Taylor, Haruhiro Toko, Eiki Takimoto, Atsuhiko T. Naito () and Issei Komuro ()
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Toshihiro Yamaguchi: Graduate School of Medicine, The University of Tokyo
Tomokazu S. Sumida: Graduate School of Medicine, The University of Tokyo
Seitaro Nomura: Graduate School of Medicine, The University of Tokyo
Masahiro Satoh: The University of Tokyo
Tomoaki Higo: Osaka University Graduate School of Medicine
Masamichi Ito: Graduate School of Medicine, The University of Tokyo
Toshiyuki Ko: Graduate School of Medicine, The University of Tokyo
Kanna Fujita: Graduate School of Medicine, The University of Tokyo
Mary E. Sweet: University of Colorado
Atsushi Sanbe: Iwate Medical University
Kenji Yoshimi: Juntendo University Graduate School of Medicine
Ichiro Manabe: Graduate School of Medicine, Chiba University
Toshikuni Sasaoka: Brain Research Institute, Niigata University
Matthew R. G. Taylor: University of Colorado
Haruhiro Toko: Graduate School of Medicine, The University of Tokyo
Eiki Takimoto: Graduate School of Medicine, The University of Tokyo
Atsuhiko T. Naito: Toho University
Issei Komuro: Graduate School of Medicine, The University of Tokyo

Nature Communications, 2020, vol. 11, issue 1, 1-8

Abstract: Abstract Pathophysiological roles of cardiac dopamine system remain unknown. Here, we show the role of dopamine D1 receptor (D1R)-expressing cardiomyocytes (CMs) in triggering heart failure-associated ventricular arrhythmia. Comprehensive single-cell resolution analysis identifies the presence of D1R-expressing CMs in both heart failure model mice and in heart failure patients with sustained ventricular tachycardia. Overexpression of D1R in CMs disturbs normal calcium handling while CM-specific deletion of D1R ameliorates heart failure-associated ventricular arrhythmia. Thus, cardiac D1R has the potential to become a therapeutic target for preventing heart failure-associated ventricular arrhythmia.

Date: 2020
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DOI: 10.1038/s41467-020-18128-x

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