Ingeborg Friehs

Outcome after reconstruction of discontinuous pulmonary arteries.

Protective effects of protein kinase C during myocardial ischemia require activation of phosphatidyl-inositol specific phospholipase C.

Dopamine treatment of postischemic contractile dysfunction rapidly induces calcium-dependent pro-apoptotic signaling.

Increased susceptibility of hypertrophied hearts to ischemic injury.

Noninvasive serial evaluation of myocardial mechanics in pressure overload hypertrophy of rabbit myocardium.

Improving results of the modified Fontan operation in patients with heterotaxy syndrome.

Postnatal increase in insulin-sensitive glucose transporter expression is associated with improved recovery of postischemic myocardial function.

Promoting angiogenesis protects severely hypertrophied hearts from ischemic injury.

Impaired insulin-signaling in hypertrophied hearts contributes to ischemic injury.

Cyclosporin A but not FK-506 protects against dopamine-induced apoptosis in the stunned heart.

Vascular endothelial growth factor delays onset of failure in pressure-overload hypertrophy through matrix metalloproteinase activation and angiogenesis.

Cardiac conduction through engineered tissue.

Vascular endothelial growth factor prevents apoptosis and preserves contractile function in hypertrophied infant heart.

Dopamine induces postischemic cardiomyocyte apoptosis in vivo: an effect ameliorated by propofol.

Age-dependent expression of VEGF isoforms and receptors in the rabbit anterior cruciate ligament.

Inhibition of glycogen synthase kinase-3beta improves tolerance to ischemia in hypertrophied hearts.

Proteasome inhibition in hypertrophied myocardium.

Myocyte apoptosis occurs early during the development of pressure-overload hypertrophy in infant myocardium.

Development of left ventricular diastolic dysfunction with preservation of ejection fraction during progression of infant right ventricular hypertrophy.

Electron transport chain dysfunction in neonatal pressure-overload hypertrophy precedes cardiomyocyte apoptosis independent of oxidative stress.

Up-regulation of soluble vascular endothelial growth factor receptor-1 prevents angiogenesis in hypertrophied myocardium.

Endogenous angiogenesis inhibitors prevent adaptive capillary growth in left ventricular pressure overload hypertrophy.

An animal model of endocardial fibroelastosis.

A highly tunable biocompatible and multifunctional biodegradable elastomer.

Pressure-overload hypertrophy of the developing heart reveals activation of divergent gene and protein pathways in the left and right ventricular myocardium.

A blood-resistant surgical glue for minimally invasive repair of vessels and heart defects.

Pressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-α-induced cardiomyocyte death.

Endocardial fibroelastosis is caused by aberrant endothelial to mesenchymal transition.

Distention of the Immature Left Ventricle Triggers Development of Endocardial Fibroelastosis: An Animal Model of Endocardial Fibroelastosis Introducing Morphopathological Features of Evolving Fetal Hypoplastic Left Heart Syndrome.

A light-reflecting balloon catheter for atraumatic tissue defect repair.

Intracoronary Delivery of Mitochondria to the Ischemic Heart for Cardioprotection.

Development of a Vascularized Heterotopic Neonatal Rat Heart Transplantation Model.

Pilomotor function is impaired in patients with Parkinson's disease: A study of the adrenergic axon-reflex response and autonomic functions.

Myocardial rescue with autologous mitochondrial transplantation in a porcine model of ischemia/reperfusion.

Vascular Endothelial Growth Factor Prevents Endothelial-to-Mesenchymal Transition in Hypertrophy.

Treating a 20 mm Hg gradient alleviates myocardial hypertrophy in experimental aortic coarctation.

Alloreactivity and allorecognition of syngeneic and allogeneic mitochondria.

A Growth-Accommodating Implant for Paediatric Applications.

Flow disturbances and progression of endocardial fibroelastosis - a case report.

Flow disturbances and the development of endocardial fibroelastosis.

Autogenous mitochondria transplantation for treatment of right heart failure.

Human endothelial colony-forming cells provide trophic support for pluripotent stem cell-derived cardiomyocytes via distinctively high expression of neuregulin-1.

Mechanical strain triggers endothelial-to-mesenchymal transition of the endocardium in the immature heart.

Endothelial-to-Mesenchymal Transition as Underlying Mechanism for the Formation of Double-Chambered Right Ventricle.

Case report: Active clinical manifestation of endocardial fibroelastosis in adolescence in a patient with mitral and aortic obstruction-histologic presence of endothelial-to-mesenchymal transformation.