טוען...
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...
שמור ב:
| הוצא לאור ב: | Cardiovasc Res |
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| Main Authors: | , , , , , , , , , , , |
| פורמט: | Artigo |
| שפה: | Inglês |
| יצא לאור: |
Oxford University Press
2017
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| נושאים: | |
| גישה מקוונת: | 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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