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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Phospholamban phosphorylation by CaMKII under pathophysiological conditions
Leticia Vittone1, Cecilia Mundina-Weilenmann, Alicia Mattiazzi
1Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, 60 y 120, 1900 La Plata, Argentina. lvittone@atlas.med.unlp.edu.ar
Calcium-calmodulin-dependent protein kinase (CaMKII) and phospholamban (PLN) phosphorylation impact heart function. CaMKII-PLN interaction aids recovery in acidosis but harms during ischemia/reperfusion and heart failure.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Cardiac Pathophysiology
Background:
- Sarcoplasmic reticulum Ca2+ ATPase (SERCA2a) activity is crucial for cardiac muscle relaxation and contraction.
- Phospholamban (PLN) regulates SERCA2a, with its phosphorylation status altering Ca2+ handling.
- Ca2+-calmodulin-dependent protein kinase (CaMKII) phosphorylates PLN at Thr17, modulating SERCA2a activity.
Purpose of the Study:
- To review the role of CaMKII and PLN phosphorylation at Thr17 in various cardiac pathophysiological conditions.
- To examine the dual role of CaMKII-PLN interaction in acidosis, ischemia/reperfusion (I/R), and heart failure (HF).
Main Methods:
- Literature review focusing on CaMKII, PLN phosphorylation at Thr17, and their effects in cardiac disease models.
- Analysis of studies investigating CaMKII activity and PLN phosphorylation in acidosis, I/R injury, and heart failure.
Main Results:
- CaMKII activation and PLN phosphorylation promote functional recovery in acidosis and stunning.
- CaMKII contributes to apoptosis and necrosis in irreversible I/R injury.
- CaMKII activity and PLN phosphorylation at Thr17 show variable changes in different heart failure models, impacting cardiac function.
Conclusions:
- CaMKII and PLN phosphorylation play complex, condition-dependent roles in cardiac function.
- Targeting CaMKII and PLN phosphorylation may offer therapeutic strategies for specific cardiac conditions.
- Further investigation is needed to elucidate the precise role of CaMKII-PLN in heart failure progression.
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