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Cardiac macrophages prevent sudden death during heart stress. 2021
Junichi Sugita, and
Katsuhito Fujiu, and
Yukiteru Nakayama, and
Takumi Matsubara, and
Jun Matsuda, and
Tsukasa Oshima, and
Yuxiang Liu, and
Yujin Maru, and
Eriko Hasumi, and
Toshiya Kojima, and
Hiroshi Seno, and
Keisuke Asano, and
Ayumu Ishijima, and
Naoki Tomii, and
Masatoshi Yamazaki, and
Fujimi Kudo, and
Ichiro Sakuma, and
Ryozo Nagai, and
Ichiro Manabe, and
Issei Komuro
Department of Cardiovascular Medicine, the University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Cardiac arrhythmias are a primary contributor to sudden cardiac death, a major unmet medical need. Because right ventricular (RV) dysfunction increases the risk for sudden cardiac death, we examined responses to RV stress in mice. Among immune cells accumulated in the RV after pressure overload-induced by pulmonary artery banding, interfering with macrophages caused sudden death from severe arrhythmias. We show that cardiac macrophages crucially maintain cardiac impulse conduction by facilitating myocardial intercellular communication through gap junctions. Amphiregulin (AREG) produced by cardiac macrophages is a key mediator that controls connexin 43 phosphorylation and translocation in cardiomyocytes. Deletion of Areg from macrophages led to disorganization of gap junctions and, in turn, lethal arrhythmias during acute stresses, including RV pressure overload and β-adrenergic receptor stimulation. These results suggest that AREG from cardiac resident macrophages is a critical regulator of cardiac impulse conduction and may be a useful therapeutic target for the prevention of sudden death.
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