Key result
PDE4D deficiency increased baseline cardiac contractility, whole-cell Ca2+ transient amplitudes, and SR Ca2+ content in mice compared to wild-type controls.
Why the study?
Does PDE4D deficiency improve baseline cardiac contractility and SR Ca2+ release in murine and human cardiomyocytes?
Population
PDE4D-deficient (PDE4D) mice at 10 to 12 weeks of age, wild-type littermate controls, and failing human…
Comparison
PDE4D deficiency, and pharmacological… vs Wild-type (WT) littermate controls
Design
Preclinical
Authors
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PDE4D modulation may enhance contractility; leaves open translation and safety for human HF therapy.
Does PDE4D deficiency improve baseline cardiac contractility and SR Ca2+ release in murine and human cardiomyocytes?
PDE4D regulates basal cAMP levels in SR microdomains containing SERCA2a-PLN, suggesting that PDE4D inhibition could have therapeutic implications for improving contractility in heart failure.
Beca et al. (2011) studied this question. PDE4D deficiency vs. Wild-type littermate controls was evaluated on Baseline cardiac contractility, whole-cell Ca2+ transient amplitudes, and SR Ca2+ content. PDE4D deficiency increased baseline cardiac contractility, whole-cell Ca2+ transient amplitudes, and SR Ca2+ content in mice compared to wild-type controls.
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