摘要
Background Studies have shown that B-blockers can improve cardiac performance in heart failure （HF） by reversing protein kinase A （PKA）-mediated sarcoplasmic reticulum （SR） Ca^2＋ leak. However, it is being strongly questioned as to whether the PKA-mediated ryanodine receptor （RyR2） hyper-phosphorylation is a critical regulator of SR Ca^2＋ leak. In this study, we used a rabbit HF model to investigate whether β-blockers affect SR Ca^2＋ leak by other potential mechanisms.
Background Studies have shown that B-blockers can improve cardiac performance in heart failure （HF） by reversing protein kinase A （PKA）-mediated sarcoplasmic reticulum （SR） Ca^2＋ leak. However, it is being strongly questioned as to whether the PKA-mediated ryanodine receptor （RyR2） hyper-phosphorylation is a critical regulator of SR Ca^2＋ leak. In this study, we used a rabbit HF model to investigate whether β-blockers affect SR Ca^2＋ leak by other potential mechanisms.
基金
This work was supported in part by grants from the Jiangsu Province ＂135 Project＂ Key Laboratory Fund （No. SK200205） in China and the National Natural Science Foundation of China （No. 30800460）.
