Abstract
Background: Atrial Fibrillation (AF) is the most common tachyarrhythmia associated with electrical, structural remodeling and contractile dysfunction, which is rooted in an impaired protein quality control (PQC) system. PQC regulates the correct folding, trafficking and degradation of proteins in cells. Heat shock proteins (HSPs) play a critical role in facilitating the PQC. Our previous studies showed that the HSP inducers geranylgeranylaceton (GGA) and its derivatives prevent contractile dysfunction in tachypaced atrial cardiomyocyte and Drosophila model for AF. Here we tested whether the potent HSP inducer GGA59 also restores contractile dysfunction in tachypaced cardiomyocytes and explored the underlying mechanisms.
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