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Institute of Physiology and Pathophysiology

Decoy oligodeoxynucleotides for the prevention of heart failure

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This research field aims at preclinically validating decoy oligodeoxynucleotides (ODNs) as a novel class of therapeutic drugs to prevent or treat heart failure.

    

Decoy ODNs, typically 15 to 20 base pairs short double-stranded DNA molecules, mimic the DNA binding site of specific regulatory proteins (transcription factors) in the genome. They interfere with the, in most cases, aberrant expression of disease-related genes by specifically binding to and, as a consequence, blocking the transcription factor controlling their expression.

 

Three different potential transcription factor drug targets are investigated. The most important criterion for choosing them is their proven involvement in the expression of genes primarily responsible for the development of various forms of terminal heart failure.

 

Members of the Division of Cardiovascular Physiology work on the design and optimization of the respective decoy ODNs. In collaboration with other groups at Heidelberg University  in vitro and in vivo model systems for the evaluation of their efficacy have been developed.

 

   

 

Aggregates of rat cardiomyocytes loaded with fluorescent decoy ODNs (red) (cell nuclei: blue)


Recent Publications

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Marfan syndrome: A therapeutic challenge for long-term care. Biochem Pharmacol. 2019 Jun;164:53-63. doi: 10.1016/j.bcp.2019.03.034. Epub 2019 Mar 27.

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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]

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Angioneurins-key regulators of blood-brain barrier integrity during hypoxic and ischemic brain injury. Prog Neurobiol. 2019 Apr 7. pii: S0301-0082(19)30039-5. doi: 10.1016/j.pneurobio.2019.03.004. [Epub ahead of print] Review.

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Chronic hypoxia changes gene expression profile of primary rat carotid body cells: consequences on the expression of NOS isoforms and ET-1 receptors. Physiol Genomics. 2019 Apr 1;51(4):109-124. doi: 10.1152/physiolgenomics.00114.2018. Epub 2019 Mar 1.

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Determination of the Maximum Velocity of Filaments in the in vitro Motility Assay. Front Physiol. 2019 Mar 27;10:289. doi: 10.3389/fphys.2019.00289. eCollection 2019.

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Genetic ablation of NFAT5/TonEBP in smooth muscle cells impairs flow- and pressure-induced arterial remodeling in mice. FASEB J. 2019 Mar;33(3):3364-3377. doi: 10.1096/fj.201801594R. Epub 2018 Nov 1.

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Priming of microglia with IFN-γ slows neuronal gamma oscillations in situ. Proc Natl Acad Sci U S A. 2019 Feb 19. pii: 201813562. doi: 10.1073/pnas.1813562116. [Epub ahead of print]

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Methylglyoxal evokes acute Ca2+ transients in distinct cell types and increases agonist-evoked Ca2+ entry in endothelial cells via CRAC channels. Cell Calcium. 2019 Mar;78:66-75. doi: 10.1016/j.ceca.2019.01.002. Epub 2019 Jan 9.

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Reduction of Transplant Vasculopathy by Intraoperative Nucleic Acid-based Therapy in a Mouse Aortic Allograft Model. Thorac Cardiovasc Surg. 2018 Oct 23. doi: 10.1055/s-0038-1673633. [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