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Phosphodiesterases 4B and 4D Differentially Regulate cAMP Signaling in Calcium Handling Microdomains of Mouse Hearts.
Cells
March 2024
Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
The ubiquitous second messenger 3',5'-cyclic adenosine monophosphate (cAMP) regulates cardiac excitation-contraction coupling (ECC) by signaling in discrete subcellular microdomains. Phosphodiesterase subfamilies 4B and 4D are critically involved in the regulation of cAMP signaling in mammalian cardiomyocytes. Alterations of PDE4 activity in human hearts has been shown to result in arrhythmias and heart failure.
View Article and Find Full Text PDFSERCA2a microdomain cAMP changes in heart failure with preserved ejection fraction.
Cardiovasc Res
March 2024
Department of Cardiology and Pneumology, Heart Research Center Göttingen, University Medical Center Göttingen, Robert-Koch-Str. 42a, 37075 Göttingen, Germany.
Remodelling of cAMP dynamics within the SERCA2a microdomain in heart failure with preserved ejection fraction caused by obesity and type 2 diabetes.
Cardiovasc Res
March 2024
Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, Martinistr. 52, D-20246 Hamburg, Germany.
Aims: Despite massive efforts, we remain far behind in our attempts to identify effective therapies to treat heart failure with preserved ejection fraction (HFpEF). Diastolic function is critically regulated by sarcoplasmic/endoplasmic reticulum (SR) calcium ATPase 2a (SERCA2a), which forms a functional cardiomyocyte (CM) microdomain where 3',5'-cyclic adenosine monophosphate (cAMP) produced upon β-adrenergic receptor (β-AR) stimulation leads to phospholamban (PLN) phosphorylation and facilitated Ca2+ re-uptake.
Methods And Results: To visualize real-time cAMP dynamics in the direct vicinity of SERCA2a in healthy and diseased myocytes, we generated a novel mouse model on the leprdb background that stably expresses the Epac1-PLN Förster resonance energy transfer biosensor.
Understanding the Role of SERCA2a Microdomain Remodeling in Heart Failure Induced by Obesity and Type 2 Diabetes.
J Cardiovasc Dev Dis
May 2022
Institute of Experimental Cardiovascular Research, University Medical Center Hamburg-Eppendorf, D-20246 Hamburg, Germany.
Obesity and type 2 diabetes (T2D) are on trend to become a huge burden across all ages. They cause harm to almost every organ, especially the heart. For decades, the incidence of heart failure with impaired diastolic function (or called heart failure with preserved ejection fraction, HFpEF) has increased sharply.
View Article and Find Full Text PDFIn Mice Subjected to Chronic Stress, Exogenous cBIN1 Preserves Calcium-Handling Machinery and Cardiac Function.
JACC Basic Transl Sci
June 2020
Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Heart failure is an important, and growing, cause of morbidity and mortality. Half of patients with heart failure have preserved ejection fraction, for whom therapeutic options are limited. Here we report that cardiac bridging integrator 1 gene therapy to maintain subcellular membrane compartments within cardiomyocytes can stabilize intracellular distribution of calcium-handling machinery, preserving diastolic function in hearts stressed by chronic beta agonist stimulation and pressure overload.
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