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- W760519778 abstract "Introduction: Abnormal sympathoexcitation worsens the prognosis of myocardial infarction (MI)-induced heart failure. We and other investigators revealed that activated brain angiotensin II type 1 receptors (AT1R) cause sympathoexcitation via oxidative stress. Previous reports, however, focused on neuronal AT1R despite the greater abundance of astrocytes than neurons in the brain, because normal astrocytes have few AT1R. Several very recent reports demonstrated that astrocytes are involved in the pathophysiology of MI-induced heart failure, but it remains unknown whether AT1R activation in the neurons or astrocytes is more crucial in MI-induced heart failure. We investigated the hypothesis that astrocytic AT1R activation plays a key role in the prognosis and left ventricular (LV) remodeling of MI-induced heart failure by genetic ablation of astrocyte-specific AT1R. Methods and Results: Using the Cre-LoxP system, we generated astrocyte-specific AT1R knockout mice (CKO-mice). At 30 days after MI, LV size and heart weight of CKO-mice were significantly smaller than those of control-MI mice (LV end-diastolic/systolic dimension: 5.0±0.1/4.5±0.1 vs. 6.1±0.1/5.6±0.1 mm, n=6, p Conclusions: Genetic ablation of astrocytic AT1R significantly improved survival prevented LV remodeling and sympathoexcitation in MI-induced heart failure. These findings indicate that astrocytic AT1R, not neuronal AT1R, have a key role in the pathophysiology of MI-induced heart failure." @default.
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- W760519778 date "2014-11-25" @default.
- W760519778 modified "2023-09-26" @default.
- W760519778 title "Abstract 13100: Genetic Ablation of Astrocyte-specific Angiotensin II Type 1 Receptors Improves Prognosis of Myocardial Infarction-Induced Heart Failure" @default.
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