Dobromir Dobrev

This paper develops a computational pipeline to predict sex-specific antiarrhythmic drug strategies for atrial fibrillation by integrating regression and mechanistic modeling of sex-specific cardiac electrophysiology.

This paper develops and validates sex-specific computational models of human atrial cardiomyocytes to investigate sex differences in atrial fibrillation mechanisms and therapeutic responses.

This study examines mitochondrial changes during atrial fibrillation in animals and humans, showing early hyperfunction and damage, and demonstrates that mitochondrial-targeted therapy can prevent adverse remodeling and AF sustainability.

This study uses computational models to show female atrial cardiomyocytes in AF have higher Ca2+-driven arrhythmia risk than males, with specific interventions identified to address these differences.

This study shows PPP1R12C overexpression in AF patients and mice leads to MLC2a dephosphorylation, reduced atrial contractility, and increased AF inducibility.