Area of research
Cardiology and Cardiovascular Medicine · Surgery
Research interest
Research focused on Inflammation and Heart failure, with related work in Ventricular remodeling, Spleen, Pressure overload. Notable publications include 'Remodeling of the Mononuclear Phagocyte Network Underlies Chronic Inflammation and Disease Progression in Heart Failure', 'Dysfunctional and Proinflammatory Regulatory T-Lymphocytes Are Essential for Adverse Cardiac Remodeling in Ischemic Cardiomyopathy', and 'CCR2+ Monocyte-Derived Infiltrating Macrophages Are Required for Adverse Cardiac Remodeling During Pressure Overload'.
CD206 <sup>+</sup> IL-4Rα <sup>+</sup> Macrophages Are Drivers of Adverse Cardiac Remodeling in Ischemic Cardiomyopathy
Splenic CD169 <sup>+</sup> Tim4 <sup>+</sup> Marginal Metallophilic Macrophages Are Essential for Wound Healing After Myocardial Infarction
Neutrophils are indispensable for adverse cardiac remodeling in heart failure
Cardiac Mesenchymal Stem Cells Promote Fibrosis and Remodeling in Heart Failure
Dysfunctional and Proinflammatory Regulatory T-Lymphocytes Are Essential for Adverse Cardiac Remodeling in Ischemic Cardiomyopathy
Optimized protocols for isolation, fixation, and flow cytometric characterization of leukocytes in ischemic hearts
CCR2+ Monocyte-Derived Infiltrating Macrophages Are Required for Adverse Cardiac Remodeling During Pressure Overload
Leukocyte iNOS is required for inflammation and pathological remodeling in ischemic heart failure
Mononuclear Phagocytes Are Dispensable for Cardiac Remodeling in Established Pressure-Overload Heart Failure
Cardiac inflammation in genetic dilated cardiomyopathy caused by MYBPC3 mutation
TNF receptor signaling inhibits cardiomyogenic differentiation of cardiac stem cells and promotes a neuroadrenergic-like fate
Remodeling of the Mononuclear Phagocyte Network Underlies Chronic Inflammation and Disease Progression in Heart Failure