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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

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TREK-1 (K2P2.1) K+ channels are suppressed in patients with atrial fibrillation and heart failure and provide therapeutic targets for rhythm control. Basic Res Cardiol. 2017 Jan;112(1):8. doi: 10.1007/s00395-016-0597-7.

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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. 2017 Jan;37(1):291-306. Epub 2016 Jan 8.

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Oxygen sensors and neuronal adaptation to ischemia. Oncotarget. 2016 Dec 15. doi: 10.18632/oncotarget.13938. [Epub ahead of print]

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Differential effects of oxytocin on mouse hippocampal oscillations in vitro. Eur J Neurosci. 2016 Dec;44(11):2885-2898. doi: 10.1111/ejn.13412. Epub 2016 Oct 14.

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Downstream effects of hippocampal sharp wave ripple oscillations on medial entorhinal cortex layer V neurons in vitro. Hippocampus. 2016 Dec;26(12):1493-1508. doi: 10.1002/hipo.22623. Epub 2016 Aug 18.

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Neuronal prolyl-4-hydroxylase 2 deficiency improves cognitive abilities in a murine model of cerebral hypoperfusion. Exp Neurol. 2016 Dec;286:93-106. doi: 10.1016/j.expneurol.2016.10.001. Epub 2016 Oct 5.

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Methodological Problems on the Way to Integrative Human Neuroscience. Front Integr Neurosci. 2016 Nov 29;10:41. Review.

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Endothelial Microparticles from Acute Coronary Syndrome Patients Induce Premature Coronary Artery Endothelial Cells Ageing and Thrombogenicity: Role of the Ang II/AT1 Receptor/NADPH Oxidase-mediated Activation of MAPKs and PI3-kinase Pathways. Circulation. 2016 Nov 7. pii: CIRCULATIONAHA.116.017513. [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