Article
Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve.
Cardiovascular research - 1 Feb 2017
Li Lei, Li Jing, Drum Benjamin M, Chen Yi, Yin Haifeng, Guo Xiaoyun, Luckey Stephen W, Gilbert Merle L, McKnight G Stanley, Scott John D, Santana L Fernando, Liu Qinghang
Abstract excerpt
AIMS: Impaired Ca2 +cycling and myocyte contractility are a hallmark of heart failure triggered by pathological stress such as hemodynamic overload. The A-Kinase anchoring protein AKAP150 has been shown to coordinate key aspects of adrenergic regulation of Ca2+cycling and excitation-contraction in cardiomyocytes. However, the role of the AKAP150 signalling complexes in the pathogenesis of heart failure has not...
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