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Institute of Physiology and Pathophysiology

Research Areas

The Hecker Working Group investigates the role of various signalling molecules in controlling the expression of mechanosensitive genes in vascular cells.

The Korff Working Group investigates mechanisms of (patho)physiological remodeling processes of arteries and veins.

Die Ullrich Working Group investigates, among other topics, the differentiation of stem cell-derived cardiomyocytes with particular focus on their electrophysiological properties.

The Wagner Working Group is interested in the role of the CD40/ CD154-mediated interaction between endothelial cells and leucocytes/ blood platelets in the early phase of chronic subacute inflammatory diseases.
Another focal point is the pathophysiological relevance of reactive oxygen species as signalling molecules in inflammatory remodelling processes in the vascular wall, in the early phase of arteriosclerosis and during the development of secondary complications in diabetes mellitus, respectively.

Scientists from the Division work on the development of novel DNA-based drugs, so-called decoy-oligonucleotides for the therapy of heart failure.


Recent Publications

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Pacemaker cell characteristics of differentiated and HCN4-transduced human mesenchymal stem cells. Life Sci. 2019 Sep 1;232:116620. doi: 10.1016/j.lfs.2019.116620. Epub 2019 Jul 7.

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Reduction of Transplant Vasculopathy by Intraoperative Nucleic Acid-based Therapy in a Mouse Aortic Allograft Model. Thorac Cardiovasc Surg. 2019 Sep;67(6):503-512. doi: 10.1055/s-0038-1673633. Epub 2018 Oct 23.

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The C-terminal HCN4 variant P883R alters channel properties and acts as genetic modifier of atrial fibrillation and structural heart disease. Biochem Biophys Res Commun. 2019 Aug 31. pii: S0006-291X(19)31679-1. doi: 10.1016/j.bbrc.2019.08.150. [Epub ahead of print]

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The neuronal oxygen-sensing pathway controls postnatal vascularization of the murine brain. FASEB J. 2019 Aug 30:fj201901385RR. doi: 10.1096/fj.201901385RR. [Epub ahead of print]

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Endothelial cell modulation of cardiomyocyte gene expression. Exp Cell Res. 2019 Aug 20:111565. doi: 10.1016/j.yexcr.2019.111565. [Epub ahead of print]

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Characterization of the Subventricular-Thalamo-Cortical Circuit in the NP-C Mouse Brain, and New Insights Regarding Treatment. Mol Ther. 2019 Aug 7;27(8):1507-1526. doi: 10.1016/j.ymthe.2019.05.008. Epub 2019 May 16.

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Functional association of a CD40 gene single nucleotide polymorphism with the pathogenesis of coronary heart disease. Cardiovasc Res. 2019 Aug 2. pii: cvz206. doi: 10.1093/cvr/cvz206. [Epub ahead of print]

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Plants Neither Possess nor Require Consciousness. Trends Plant Sci. 2019 Aug;24(8):677-687. doi: 10.1016/j.tplants.2019.05.008. Epub 2019 Jul 3.

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Augmentation of myocardial If dysregulates calcium homeostasis and causes adverse cardiac remodeling. Nat Commun. 2019 Jul 23;10(1):3295. doi: 10.1038/s41467-019-11261-2.

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15-Deoxy-Δ12,14-Prostaglandin J2 Reinforces the Anti-Inflammatory Capacity of Endothelial Cells with a Genetically Determined Nitric Oxide Deficit. Circ Res. 2019 Jul 19;125(3):282-294. doi: 10.1161/CIRCRESAHA.118.313820. Epub 2019 Jun 19.

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Persistent increase in ventral hippocampal long-term potentiation by juvenile stress: A role for astrocytic glutamine synthetase. Glia. 2019 Jul 17. doi: 10.1002/glia.23683. [Epub ahead of print]

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Angioneurins-key regulators of blood-brain barrier integrity during hypoxic and ischemic brain injury. Prog Neurobiol. 2019 Jul;178:101611. doi: 10.1016/j.pneurobio.2019.03.004. Epub 2019 Apr 7. Review.

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Somatic mutations and promotor methylation of the ryanodine receptor 2 is a common event in the pathogenesis of head and neck cancer. Int J Cancer. 2019 May 28. doi: 10.1002/ijc.32481. [Epub ahead of print]

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TRPC channels are not required for graded persistent activity in entorhinal cortex neurons. Hippocampus. 2019 Apr 19. doi: 10.1002/hipo.23094. [Epub ahead of print]


Institute of
Physiology and Pathophysiology

Heidelberg University

Im Neuenheimer Feld 326

69120 Heidelberg

Germany

Phone:+49 6221 54-4035
Fax:+49 6221 54-4038
E-mail:sekretariat.hecker@
physiologie.uni-heidelberg.de