J. Drenckhahn

发表

Arrhythmogenic right ventricular cardiomyopathy type 5 is a fully penetrant, lethal arrhythmic disorder caused by a missense mutation in the TMEM43 gene.

Sean Connors, Patrick S Parfrey, Barry Gallagher, 2008, American journal of human genetics.

Growth plasticity of the embryonic and fetal heart

J. Drenckhahn, 2009, BioEssays : news and reviews in molecular, cellular and developmental biology.

Consequences of variations in litter size on postnatal cardiac growth

J. Drenckhahn, 2009 .

Dietary protein restriction throughout intrauterine and postnatal life results in potentially beneficial myocardial tissue remodeling in the adult mouse heart

L. Thierfelder, C. Jux, A. Uebing, 2019, Scientific Reports.

Impact of Intrauterine Growth Restriction on the Capillarization of the Early Postnatal Rat Heart

M. Black, M. Wlodek, J. Drenckhahn, 2019, Anatomical record.

Impaired myocardial development resulting in neonatal cardiac hypoplasia alters postnatal growth and stress response in the heart.

T. Cox, Jette Strasen, F. Blaschke, 2015, Cardiovascular research.

Heart development: mitochondria in command of cardiomyocyte differentiation.

J. Drenckhahn, 2011, Developmental cell.

Preserved Heart Function after Left Ventricular Pressure Overload in Adult Mice Subjected to Neonatal Cardiac Hypoplasia

F. Blaschke, L. Thierfelder, C. Jux, 2017, The Thoracic and Cardiovascular Surgeon.

Prenatal Mechanistic Target of Rapamycin Complex 1 (m TORC1) Inhibition by Rapamycin Treatment of Pregnant Mice Causes Intrauterine Growth Restriction and Alters Postnatal Cardiac Growth, Morphology, and Function

L. Thierfelder, C. Jux, J. Drenckhahn, 2017, Journal of the American Heart Association.

3‐D Imaging of Biomedical Samples

K. Bambery, B. Wood, D. McNaughton, 2009 .

Inhibition of mitochondrial respiration has fundamentally different effects on proliferation, cell survival and stress response in immature versus differentiated cardiomyocyte cell lines

Vijay Singh, C. Jux, H. Kehl, 2022, Frontiers in Cell and Developmental Biology.

Transcriptional profiling of regenerating embryonic mouse hearts

H. Schulz, L. Thierfelder, J. Drenckhahn, 2016, Genomics data.

Activation of Peroxisome Proliferator–Activated Receptor-&dgr; as Novel Therapeutic Strategy to Prevent In-Stent Restenosis and Stent Thrombosis

B. Pieske, S. Ylä-Herttuala, F. Blaschke, 2016, Arteriosclerosis, thrombosis, and vascular biology.

Mutations in Sarcomere Protein Genes in Left Ventricular Noncompaction

F. Berger, E. Oechslin, R. Jenni, 2008, Circulation.

Fine mapping of the 1p36 deletion syndrome identifies mutation of PRDM16 as a cause of cardiomyopathy.

G. Musso, R. Siebert, S. Cook, 2013, American journal of human genetics.

Embryonic cardiomyocytes can orchestrate various cell protective mechanisms to survive mitochondrial stress.

S. Donath, F. Blaschke, H. Schulz, 2016, Journal of molecular and cellular cardiology.

The impact of implantable cardioverter-defibrillator therapy on survival in autosomal-dominant arrhythmogenic right ventricular cardiomyopathy (ARVD5).

A. Bassett, P. Parfrey, E. Dicks, 2005, Journal of the American College of Cardiology.

Compensatory growth of healthy cardiac cells in the presence of diseased cells restores tissue homeostasis during heart development.

R. Harvey, T. Cox, D. Thorburn, 2008, Developmental cell.

Cardiomyocyte hyperplasia and immaturity but not hypertrophy are characteristic features of patients with RASopathies.

S. Dimmeler, W. Abplanalp, D. John, 2023, Journal of molecular and cellular cardiology.

Mutations in Sarcomere Protein Genes in Left Ventricular Noncompaction

F. Berger, E. Oechslin, R. Jenni, 2008, Circulation.

Cardiomyocyte hyperplasia and immaturity but not hypertrophy are characteristic features of patients with RASopathies.

S. Dimmeler, W. Abplanalp, D. John, 2023, Journal of molecular and cellular cardiology.