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- URN zum Zitieren dieses Dokuments:
- urn:nbn:de:bvb:355-epub-587483
- DOI zum Zitieren dieses Dokuments:
- 10.5283/epub.58748
Zusammenfassung
Aims Hyperactivity of Ca2+/calmodulin-dependent protein kinase II (CaMKII) has emerged as a central cause of pathologic remodelling in heart failure. It has been suggested that CaMKII-induced hyperphosphorylation of the ryanodine receptor 2 (RyR2) and consequently increased diastolic Ca2+ leak from the sarcoplasmic reticulum (SR) is a crucial mechanism by which increased CaMKII activity leads to ...
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