| Autor: |
Baier, Maria J., Noack, Jannis, Seitz, Mark Tilmann, Maier, Lars S., Neef, Stefan |
| Rok vydání: |
2021 |
| Předmět: |
|
| DOI: |
10.5283/epub.51656 |
| Popis: |
Adrenergic stimulation, while being the central mechanism of cardiac positive inotropy, is a universally acknowledged inductor of undesirable sarcoplasmic reticulum (SR) Ca2+ leak. However, the exact mechanisms for this remained unspecified so far. This study shows that Ca2+/calmodulin-dependent protein kinase II (CaMKII)-specific phosphorylation of ryanodine receptor type 2 at Ser-2814 is the pivotal mechanism by which SR Ca2+ leak develops downstream of ��1-adrenergic stress by increase of the leak/load relationship. Cardiomyocytes with a Ser-2814 phosphoresistant mutation (S2814A) were protected from isoproterenol-induced SR Ca2+ leak and consequently displayed improved postrest potentiation of systolic Ca2+ release under adrenergic stress compared to littermate wild-type cells. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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