Excitation-contraction coupling, cardiomyocyte electrophysiology, and transcriptome profiles in two HFpEF murine models: Etiology and sex-dependent differences
Analyses reveal diastolic dysfunction and distinct gene expression in HFpEF models, indicating etiology and sex differences.
Key Points
The aim was to compare mechanisms of excitation-contraction coupling, electrophysiology, and gene transcription in HFpEF models with a focus on sex differences.
Utilized two HFpEF murine models: HFD+L-NAME and db/db+Aldo.
Conducted morphometry, echocardiography, cellular electrophysiology, and RNA-sequencing.
Analysed diastolic dysfunction and action potential changes across sexes in both models.
Diastolic dysfunction was more severe in db/db+Aldo mice, especially in females.
Marked proarrhythmic action potential changes were observed in db/db+Aldo mice of both sexes.
Distinctive gene expression profiles were identified between the two HFpEF models.