Area of research
Cardiology and Cardiovascular Medicine · Rheumatology
Research interest
Research interests include Cardiac Fibrosis and Remodeling, GDF15 and Related Biomarkers, IL-33, ST2, and ILC Pathways, and Heart Failure Treatment and Management.
Extracellular BRICK1 drives heart repair after myocardial infarction in mice.
RHOT Proteins Link Mitochondrial Motility to Cardiomyocyte Sarcomere Maturation.
Mitotane treatment of adrenocortical carcinoma induces tumoural secretion of GDF-15: impact on poor prognosis and impaired responsiveness to immunotherapy.
Identification of myeloid-derived growth factor as a mechanically-induced, growth-promoting angiocrine signal for human hepatocytes
Hypoxia Attenuates Pressure Overload‐Induced Heart Failure
Identification of myeloid-derived growth factor as a mechanically-induced, growth-promoting angiocrine signal for human hepatocytes.
Hypoxia Attenuates Pressure Overload-Induced Heart Failure.
Cysteine-rich with EGF-like domains 2 (CRELD2) is an endoplasmic reticulum stress-inducible angiogenic growth factor promoting ischemic heart repair.
Growth differentiation factor 15 and cardiovascular risk: individual patient meta-analysis.
Cardiac Troponin I-Interacting Kinase Affects Cardiomyocyte S-Phase Activity but Not Cardiomyocyte Proliferation.
Pre-emptive iron supplementation prevents myocardial iron deficiency and attenuates adverse remodelling after myocardial infarction.
Meteorin-like promotes heart repair through endothelial KIT receptor tyrosine kinase
Meteorin-like promotes heart repair through endothelial KIT receptor tyrosine kinase.
Growth differentiation factor 15 and cardiovascular risk: individual patient meta-analysis
Skeletal muscle derived Musclin protects the heart during pathological overload
Biomarker-Based Prediction of Recurrent Ischemic Events in Patients With Acute Coronary Syndromes
Integrated analyses of growth differentiation factor-15 concentration and cardiometabolic diseases in humans
Response by Wollert to Letter Regarding Article, "Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure".
Corrigendum to: A mouse model of cardiogenic shock.
Myeloid-Derived Growth Factor Protects Against Pressure Overload–Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca <sup>2+</sup> -ATPase Expression in Cardiomyocytes
Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca<sup>2+</sup>-ATPase Expression in Cardiomyocytes.
Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesis
A mouse model of cardiogenic shock.
Angiogenesis after acute myocardial infarction
Angiogenesis after acute myocardial infarction
Molecular imaging-guided repair after acute myocardial infarction by targeting the chemokine receptor CXCR4
Molecular imaging-guided repair after acute myocardial infarction by targeting the chemokine receptor CXCR4
Cardiac Iron Concentration in Relation to Systemic Iron Status and Disease Severity in Non-Ischaemic Heart Failure with Reduced Ejection Fraction
C-X-C Motif Chemokine Receptor 4 Blockade Promotes Tissue Repair After Myocardial Infarction by Enhancing Regulatory T Cell Mobilization and Immune-Regulatory Function
Continuous WNT Control Enables Advanced hPSC Cardiac Processing and Prognostic Surface Marker Identification in Chemically Defined Suspension Culture