@article{oai:soar-ir.repo.nii.ac.jp:02001244,
 author = {Kashihara, Toshihide and Kawagishi, Hiroyuki and Nakada, Tsutomu and Numaga-Tomita, Takuro and Kadota, Shin and Wolf, Elena E. and Du, Cheng-Kun and Shiba, Yuji and Morimoto, Sachio and Yamada, Mitsuhiko},
 issue = {11},
 journal = {JACC. Basic to translational science},
 month = {Nov},
 note = {The treatment of pediatric heart failure is a long-standing unmet medical need. Angiotensin II supports mammalian perinatal circulation by activating cardiac L-type Ca2+ channels through angiotensin type 1 receptor (AT1R) and β-arrestin. TRV027, a β-arrestin-biased AT1R agonist, that has been reported to be safe but not effective for adult patients with heart failure, activates the AT1R/β-arrestin pathway. We found that TRV027 evokes a long-acting positive inotropic effect specifically on immature cardiac myocytes through the AT1R/β-arrestin/L-type Ca2+ channel pathway with minimum effect on heart rate, oxygen consumption, reactive oxygen species production, and aldosterone secretion. Thus, TRV027 could be utilized as a valuable drug specific for pediatric heart failure., Article, JACC. Basic to translational science 5(11) : 1057-1069(2020)},
 pages = {1057--1069},
 title = {β-Arrestin-Biased AT1 Agonist TRV027 Causes a Neonatal-Specific Sustained Positive Inotropic Effect Without Increasing Heart Rate},
 volume = {5},
 year = {2020}
}