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Institute of Physiology and Pathophysiology

Korff Group

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Biomechanically Triggered Remodeling in the Cardiovascular System


Cardiovascular research belongs to the most rapidly growing biomedical disciplines as it deals predominantly with diseases that are the leading cause of death in industrial countries. These include, but are not limited to coronary heart disease, cardiomyopathy, hypertension and arterial disease, heart hypertrophy, heart failure, arteriosclerosis, stroke, peripheral arterial disease and varicosis.


The focus of my group is on the investigation of biomechanically triggered mechanisms which either promote cardiovascular diseases or at least partially compensate their harmful effects. Therefore, we are especially interested in the analysis of cardiac insufficiency, development of arteriosclerotic lesions, hypertension-induced arterial remodeling, varicose vein formation as well as arteriogenesis, the formation of collateral arteries from preexisting arterioles to compensate the occlusion of a conduit artery.


All of these pathophysiological processes are basically associated with the adaptive or maladaptive remodeling of the cardiac or vessel wall, which is strictly dependent on phenotypic changes of the corresponding tissue-specific cells, namely cardiomyocytes, endothelial and vascular smooth muscle cells. Against this background, our working hypothesis is that biomechanical deformation of cells in cardiovascular tissues is an important determinant of their phenotype and sufficient to initiate pathophysiological remodeling processes.




Biomechanical deformation (stretch) of smooth muscle cells is determined by circumferential wall stress (St )

Wall stress is defined by the law of Laplace. Its chronic increase (e.g. by a hypertension-induced increase in the transmural pressure difference) induces the deformation (stretch) of endothelial cells (EC) and vascular smooth muscle cells (SMC) in the blood vessel wall, which may elicit pathophysiological remodeling processes of the cardiac or vessel wall.



In fact, hypertension-induced arterial remodeling, arteriogenesis, (afterload-related) cardiac insufficiency, endothelial dysfunction at arteriosclerotic predilection sites, as well as varicose vein formation are all associated with or elicited by a chronic increase in wall stress.




Our previous work encompasses several topics of cardiovascular research and has underlined the relevance of this biomechanical force for changes in the phenotype of endothelial and vascular smooth muscle cells.



Stretch is an important trigger of vascular remodeling processes.



Korff et al., Circulation 2007
Korff et al., Blood 2008
Demicheva et al., Circ. Res. 2008

Hypertension impairs expression of “contractile gene products” in vascular SMCs.



Pfisterer et al., Cardiovasc. Res., 2012

Wall stress is sufficient to trigger varicose vein development.



Feldner et al., FASEB J, 2011



To achieve a better understanding of the intracellular signaling mechanisms that are triggered by an increase in wall stress, our experimental portfolio includes multiple in vitro and in vivo techniques: In vitro we utilize the FlexCell system, which allows us to expose cultured cells to defined levels of cyclic stretch. This system is used for basic mechanistic studies which help us to identify new stretch-regulated target molecules. In addition, we perfuse isolated mouse arteries and veins under defined pressure/flow conditions in order to closely mimic the in vivo environment.

In vivo, we employ various hypertension models and the hindlimb ischemia model in which the occlusion of the femoral artery induces arteriogenic remodeling of the collateral arterioles. We also take advantage of our specialized mouse auricle artery/vein ligation models, which allow for the easy visualization and measurement of changes in the vascular architecture and the local transdermal application of experimental reagents (e.g. decoy oligodeoxynucleotides).


Recent Publications


Selective vulnerability of αOFF retinal ganglion cells during onset of autoimmune optic neuritis. Neuroscience. 2018 Nov 21;393:258-272. doi: 10.1016/j.neuroscience.2018.07.040. Epub 2018 Aug 1.


Genetic ablation of NFAT5/TonEBP in smooth muscle cells impairs flow- and pressure-induced arterial remodeling in mice. FASEB J. 2018 Nov 1:fj201801594R. doi: 10.1096/fj.201801594R. [Epub ahead of print]


Synaptic entrainment of ectopic action potential generation in hippocampal pyramidal neurons.  J Physiol. 2018 Nov;596(21):5237-5249. doi: 10.1113/JP276720. Epub 2018 Sep 19.


The Long Noncoding RNA Cancer Susceptibility 9 and RNA Binding Protein Heterogeneous Nuclear Ribonucleoprotein L Form a Complex and Coregulate Genes Linked to AKT Signaling. Hepatology. 2018 Nov;68(5):1817-1832. doi: 10.1002/hep.30102. Epub 2018 Oct 12.


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]


Early appearance and spread of fast ripples in the hippocampus in a model of cortical traumatic brain injury. J Neurosci. 2018 Oct 17;38(42):9034-9046. doi: 10.1523/JNEUROSCI.3507-17.2018. Epub 2018 Sep 6.


High-fat diet suppresses the positive effect of creatine supplementation on skeletal muscle function by reducing protein expression of IGF-PI3K-AKT-mTOR pathway. PLoS One. 2018 Oct 4;13(10):e0199728. doi: 10.1371/journal.pone.0199728. eCollection 2018.


Alcohol reduces muscle fatigue through atomistic interactions with nicotinic receptors. Commun Biol. 2018 Oct 3;1:159. doi: 10.1038/s42003-018-0157-9. eCollection 2018.


Possible neurotoxicity of the anesthetic propofol: evidence for the inhibition of complex II of the respiratory chain in area CA3 of rat hippocampal slices. Arch Toxicol. 2018 Oct;92(10):3191-3205. doi: 10.1007/s00204-018-2295-8. Epub 2018 Aug 24.


Endothelial progenitor cells accelerate endothelial regeneration in an in vitro model of Shigatoxin-2a-induced injury via soluble growth factors. Am J Physiol Renal Physiol. 2018 Oct 1;315(4):F861-F869. doi: 10.1152/ajprenal.00633.2017. Epub 2018 Mar 7.


Strategy for marker-based differentiation of pro- and anti-inflammatory macrophages using matrix-assisted laser desorption/ionization mass spectrometry imaging. Analyst. 2018 Sep 10;143(18):4273-4282. doi: 10.1039/c8an00659h. Epub 2018 Jul 20.


Recent advances in hippocampal structure and function. Cell Tissue Res. 2018 Sep;373(3):521-523. doi: 10.1007/s00441-018-2913-z. Epub 2018 Aug 20. doi: 10.1007/s00441-018-2913-z. Editorial. No abstract available.


Electrical coupling between hippocampal neurons: contrasting roles of principal cell gap junctions and interneuron gap junctions. Cell Tissue Res. 2018 Sep;373(3):671-691. doi: 10.1007/s00441-018-2881-3. Epub 2018 Aug 15. Review.


Metabolic modulation of neuronal gamma-band oscillations. Pflugers Arch2018 Sep;470(9):1377-1389. doi: 10.1007/s00424-018-2156-6. Epub 2018 May 28.


The VAMP-associated protein VAPB is required for cardiac and neuronal pacemaker channel function. FASEB J. 2018 Jun 7:fj201800246R. doi: 10.1096/fj.201800246R. [Epub ahead of print]

Institute of
Physiology and Pathophysiology

Heidelberg University

Im Neuenheimer Feld 326

69120 Heidelberg


Phone:+49 6221 54-4035
Fax:+49 6221 54-4038