Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve

AIMS: Impaired Ca(2 + )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 Ca(2+ )cycling and excitation–contractio...

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Detalhes bibliográficos
Publicado no:Cardiovasc Res
Main Authors: 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
Formato: Artigo
Idioma:Inglês
Publicado em: Oxford University Press 2017
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Original Articles
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC5340143/
https://ncbi.nlm.nih.gov/pubmed/27856611
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/cvr/cvw221
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