Key result
Prior S-nitrosylation of CaMKIIδ at cysteine-273 by NO donors limited subsequent β-adrenergic receptor-induced arrhythmias, whereas S-nitrosylation at cysteine-290 worsened or sustained them.
Why the study?
Although nitric oxide donors are used clinically for cardioprotection, it is unknown how they modulate proarrhythmic CaMKII to alter cardiac arrhythmia incidence.
Population
Isolated cardiomyocytes and Langendorff-perfused hearts from WT, CaMKIIδ-KO, CaMKIIδ-C273S, and CaMKIIδ-C290A mice
Comparison
NO donors (GSNO, sodium nitroprusside) and isoproterenol across WT and mutant mouse models
Design
Preclinical laboratory study
Authors
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Timing of NO donor effects on CaMKIIδ may modulate arrhythmia risk; hypothesis-generating and leaves open clinical translation.
Prior S-nitrosylation of CaMKIIδ at cysteine-273 limits β-adrenergic receptor-induced arrhythmias, whereas S-nitrosylation at cysteine-290 may worsen them, highlighting timing-dependent effects of NO donors.
Power et al. (2023) studied Cardiac arrhythmias. NO donors (GSNO, sodium nitroprusside) and isoproterenol vs. Wild-type vs knock-out/knock-in mice was evaluated on Ca2+ spark frequency and arrhythmias. Prior S-nitrosylation of CaMKIIδ at cysteine-273 by NO donors limited subsequent β-adrenergic receptor-induced arrhythmias, whereas S-nitrosylation at cysteine-290 worsened or sustained them.
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