Area of research
Cardiology and Cardiovascular Medicine · Molecular Biology
Research interest
Research interests include Cardiac electrophysiology and arrhythmias, Ion channel regulation and function, Cardiac Fibrosis and Remodeling, and Cardiovascular Function and Risk Factors.
Metabolic Reprogramming: A Byproduct or a Driver of Cardiomyocyte Proliferation?
Protein Kinase A Is a Master Regulator of Physiological and Pathological Cardiac Hypertrophy.
RNA-Binding Protein LIN28a Regulates New Myocyte Formation in the Heart Through Long Noncoding RNA-H19.
Systemic Hypoxemia Induces Cardiomyocyte Hypertrophy and Right Ventricular Specific Induction of Proliferation
Systemic Hypoxemia Induces Cardiomyocyte Hypertrophy and Right Ventricular Specific Induction of Proliferation.
Functional LTCC-β<sub>2</sub>AR Complex Needs Caveolin-3 and Is Disrupted in Heart Failure.
miR-182/183-Rasa1 axis induced macrophage polarization and redox regulation promotes repair after ischemic cardiac injury
Combining three independent pathological stressors induces a heart failure with preserved ejection fraction phenotype.
Effects of maternal hypothyroidism on postnatal cardiomyocyte proliferation and cardiac disease responses of the progeny.
Will Induction of Transient Myocyte Proliferation Be a Regenerative Therapy?
Sex-specific responses to slow progressive pressure overload in a large animal model of HFpEF.
HDAC Inhibition Reverses Preexisting Diastolic Dysfunction and Blocks Covert Extracellular Matrix Remodeling
HDAC Inhibition Reverses Preexisting Diastolic Dysfunction and Blocks Covert Extracellular Matrix Remodeling.
Cortical bone stem cell-derived exosomes' therapeutic effect on myocardial ischemia-reperfusion and cardiac remodeling.
Cortical bone stem cells modify cardiac inflammation after myocardial infarction by inducing a novel macrophage phenotype.
Cardiac Remodeling During Pregnancy With Metabolic Syndrome: Prologue of Pathological Remodeling.
Abstract MP202: The Effects Of Maternal Hypothyroidism On Fetal And Adult Cardiac Function
Response to Letter Regarding Article, "Cardiac Remodeling During Pregnancy With Metabolic Syndrome: Prologue of Pathological Remodeling".
Thomas L. Force, MD: 1951-2020
HDAC inhibition improves cardiopulmonary function in a feline model of diastolic dysfunction.
Circular RNA CircFndc3b modulates cardiac repair after myocardial infarction via FUS/VEGF-A axis
Cardiomyocyte PKA Ablation Enhances Basal Contractility While Eliminates Cardiac β-Adrenergic Response Without Adverse Effects on the Heart
Cortical Bone Derived Stem Cells for Cardiac Wound Healing.
New Myocyte Formation in the Adult Heart
Cardiomyocyte Regeneration: A Consensus Statement.
The mitochondrial Na+/Ca2+ exchanger is essential for Ca2+ homeostasis and viability
Neonatal Transplantation Confers Maturation of PSC-Derived Cardiomyocytes Conducive to Modeling Cardiomyopathy
Caveolae-localized L-type Ca2+ channels do not contribute to function or hypertrophic signalling in the mouse heart
Increasing T‐type calcium channel activity by β‐adrenergic stimulation contributes to β‐adrenergic regulation of heart rates
Protein Kinase C Inhibition With Ruboxistaurin Increases Contractility and Reduces Heart Size in a Swine Model of Heart Failure With Reduced Ejection Fraction