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- W4387003010 abstract "The purpose of this study was to characterize the role of β1-AR signaling and its cross-talk between cardiac renin-angiotensin system and thyroid-hormone-induced cardiac hypertrophy. T3 was administered at 0.5 mg·kg-1·day-1 for 10 days in β1-KOT3 and WTT3 groups, while control groups received vehicle alone. Echocardiography and myocardial histology was performed; cardiac and serum ANGI/ANGII and ANP and cardiac levels of p-PKA, p-ERK1/2, p-p38-MAPK, p-AKT, p-4EBP1, and ACE were measured. WTT3 showed decreased IVSTd and increased LVEDD versus WTsal (p < 0.05). β1-KOT3 exhibited lower LVEDD and higher relative IVSTd versus β1-KOsal, the lowest levels of ejection fraction, and the highest levels of cardiomyocyte diameter (p < 0.05). Cardiac ANP levels decreased in WTT3 versus β1-KOT3 (p < 0.05). Cardiac ACE expression was increased in T3-treated groups (p < 0.05). Phosphorylated-p38 MAPK levels were higher in WTT3 versus WTsal or β1-KOT3, p-4EBP1 was elevated in β1-KO animals, and p-ERK1/2 was up-regulated in β1-KOT3. These findings suggest that β1-AR signaling is crucial for TiCH." @default.
- W4387003010 created "2023-09-26" @default.
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- W4387003010 date "2023-09-25" @default.
- W4387003010 modified "2023-10-12" @default.
- W4387003010 title "Thyroid hormone induces restrictive cardiomyopathy in β1-adrenoceptor knockout mice" @default.
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- W4387003010 doi "https://doi.org/10.1139/cjpp-2023-0153" @default.
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