Increased CaMKII activation and contrast changes of cardiac β1-and β3-Adrenergic signaling pathways in a humanized angiotensinogen model of hypertension.

Heliyon(2023)

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摘要
LV myocyte CaMKIIδ overactivation with associated contrast changes in β-AR and β-AR may be the key molecular mechanism for the abnormal contractile phenotype and β-AR desensitization in this humanized model of hypertension.
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关键词
Calcium-calmodulin-dependent protein kinase, type II, Hypertension, Cardiomyocyte, Transgenic models, 13-adrenergic reserve, Angiotensinogen, Renin-angiotensin system, Heart failure
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