Marc N. Hirt

Human engineered heart tissue as a versatile tool in basic research and preclinical toxicology.

Increased afterload induces pathological cardiac hypertrophy: a new in vitro model.

Contractile abnormalities and altered drug response in engineered heart tissue from Mybpc3-targeted knock-in mice.

Cardiac tissue engineering: state of the art.

Automated analysis of contractile force and Ca2+ transients in engineered heart tissue.

Functional improvement and maturation of rat and human engineered heart tissue by chronic electrical stimulation.

Deciphering the microRNA signature of pathological cardiac hypertrophy by engineered heart tissue- and sequencing-technology.

General practitioners' adherence to chronic heart failure guidelines regarding medication: the GP-HF study.

DNA methylation in an engineered heart tissue model of cardiac hypertrophy: common signatures and effects of DNA methylation inhibitors.

Spontaneous Formation of Extensive Vessel-Like Structures in Murine Engineered Heart Tissue.

Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.

Human Engineered Heart Tissue: Analysis of Contractile Force.

Glycoproteomics Reveals Decorin Peptides With Anti-Myostatin Activity in Human Atrial Fibrillation.

Human iPSC-derived cardiomyocytes cultured in 3D engineered heart tissue show physiological upstroke velocity and sodium current density.

Pharmacological inhibition of DNA methylation attenuates pressure overload-induced cardiac hypertrophy in rats.

S100A4 as a Target of the E3-Ligase Asb2β and Its Effect on Engineered Heart Tissue.

Toward Second-Generation Cardiomyogenic and Anti-cardiofibrotic 1,4-Dihydropyridine-Class TGFβ Inhibitors.

Blockade of miR-140-3p prevents functional deterioration in afterload-enhanced engineered heart tissue.

Long Noncoding RNA-Enriched Vesicles Secreted by Hypoxic Cardiomyocytes Drive Cardiac Fibrosis.

A magnetics-based approach for fine-tuning afterload in engineered heart tissues.

Phosphomimetic cardiac myosin-binding protein C partially rescues a cardiomyopathy phenotype in murine engineered heart tissue.

Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction.