Select languageSelect language
Institute of Physiology and Pathophysiology

Cardiovascular Physiology

Director

 

Prof. Dr. Markus Hecker

 

Phone:

+49 6221 54-4036/4035

Fax:

+49 6221 54-4038

E-Mail:

hecker@physiologie.uni-heidelberg.de

 

Secretary

 

Barbara Richards

 

Phone:

+49 6221 54-4035

Fax:

+49 6221 54-4038

E-Mail:

sekretariat.hecker@physiologie.uni-heidelberg.de

Our Field of Research

Our research focuses on the molecular mechanisms underlying pathophysiological and physiological remodelling processes in the cardiovascular system, to define new therapeutic aproaches for cardiovascular disease.

 

At present five working groups and one project team concentrate on various research areas within this field.

 

Scientists of the division are also integrated in a number of local and national research centers and networks:

   


Recent Publications

*

Amyloid Precursor Protein Protects Neuronal Network Function after Hypoxia via Control of Voltage-Gated Calcium Channels. J Neurosci. 2016 Aug 10;36(32):8356-71. doi: 10.1523/JNEUROSCI.4130-15.2016.

*

Downstream effects of hippocampal sharp wave ripple oscillations on medial entorhinal cortex layer V neurons in vitro. Hippocampus. 2016 Aug 1. doi: 10.1002/hipo.22623. [Epub ahead of print]

*

Essential light chain S195 phosphorylation is required for cardiac adaptation under physical stress. Cardiovasc Res. 2016 Jul 1;111(1):44-55. doi: 10.1093/cvr/cvw066. Epub 2016 Mar 24.

*

Neuronal deficiency of HIF prolyl 4-hydroxylase 2 in mice improves ischemic stroke recovery in an HIF dependent manner. Neurobiol Dis. 2016 Jul;91:221-35. doi: 10.1016/j.nbd.2016.03.018. Epub 2016 Mar 19.

*

Energy and Potassium Ion Homeostasis during Gamma Oscillations. Front Mol Neurosci. 2016 Jun 16;9:47. doi: 10.3389/fnmol.2016.00047. eCollection 2016. Review.

*

Satellite microglia display spontaneous electrical activity uncorrelated with activity of the attached neuron. Eur J Neurosci. 2016 Jun;43(11):1523-34. doi: 10.1111/ejn.13256. Epub 2016 May 21.

*

Fumaric acid esters promote neuronal survival upon ischemic stress through activation of the Nrf2 but not HIF-1 signaling pathway. Neuropharmacology. 2016 Jun;105:228-40. doi: 10.1016/j.neuropharm.2016.01.023. Epub 2016 Jan 19.

*

KCC2 knockdown impairs glycinergic synapse maturation in cultured spinal cord neurons. Histochem Cell Biol. 2016 Jun;145(6):637-46. doi: 10.1007/s00418-015-1397-0. Epub 2016 Jan 16.

*

The interneuron energy hypothesis: implications for brain disease. Neurobiol Dis. 2016 Jun;90:75-85. doi: 10.1016/j.nbd.2015.08.005. Epub 2015 Aug 16.

*

Neuronal HIF-1α and HIF-2α deficiency improves neuronal survival and sensorimotor function in the early acute phase after ischemic stroke. J Cereb Blood Flow Metab. 2016 Jan 8. pii: 0271678X15624933. [Epub ahead of print]


Institute of
Physiology and Pathophysiology

Heidelberg University

Im Neuenheimer Feld 326

69120 Heidelberg

Germany

Phone:+49 6221 54-4056
Fax:+49 6221 54-6364
E-mail:susanne.bechtel@
physiologie.uni-heidelberg.de