The overall goal of our research is to develop novel mathematical models and computational/statistical tools to investigate the molecular and sub-cellular mechanisms of complex cardiovascular diseases such as heart failure, atrial fibrillation, sick sinus syndrome, hypertension, and diabetes.
A common theme of our research is in utilizing these computational frameworks to quantitatively assess the role and crosstalk of ion homeostasis and intracellular signaling pathways in health and disease. We leverage this understanding to identify therapeutic targets, inform treatment strategies, and predict the outcome of pharmacological treatment.
Specific research areas include:
Dysregulation of ventricular excitation-contraction coupling in heart failure
Effect of sex differences on cardiac electrophysiology and pharmacology
Inter-subject variability and patient-specific therapeutic approaches
Mechanisms and treatments for supraventricular arrhythmias
Regulation of contractility in vascular smooth muscle cells
Funding:
01/2025-12/2028
NIH/NHLBI R01HL176651
Calcium driven fibroblast dysregulation in human atrial profibrotic remodeling
Co-I (PI: Dr. Eleonora Grandi)
07/2024-05/2029
NIH/NHLBI R01HL171057
Phenotype-specific models, mechanisms, and treatment of heart failure with preserved ejection fraction (HFpEF)
PI
01/2024-12/2028
NIH/NHLBI R01HL171586
Phosphodiesterase 1 (PDE1) regulation of myocardial calcium and function
Co-I (PI: Dr. Grace Muller)
12/2023-11/2027
NIH/NHLBI R01HL171014
Mechanisms of vascular smooth muscle (VSM) dysfunction in diabetes and HFpEF
Co-I (PI: Dr. Manuel Navedo; co-PI: Dr. Madeline Nieves-Cintrón)