Cardiovascular Pharmacology

The Cardiovascular Pharmacology group aims to identify molecular key signals for cardiovascular diseases. Their work mainly focuses on heart failure (cardiac insufficiency) and cardiac hypertrophy. To find new strategies for reducing the high mortality and prevalence of these diseases, it is necessary to detect them early and influence their progression. However, this is only feasible when the molecular causes are cleared up.

When the heart is exposed to increased stress, caused for instance by high blood pressure, it reacts with increased growth (hypertrophy) of the cardiac muscle. Thus it is able to resist increased stress and to maintain its regular performance up to a certain point. However, the process can turn negative if the heart is not relieved: Too much growth causes muscle cells to die; the heart becomes scarred and will sustain lasting damage.

From a physiological point of view, these processes are well understood, but on the molecular level it remains unclear what exactly happens in the cells and how the diseases might be stopped. In earlier studies the group has already been able to find potential therapy approaches. For instance, the kinases ERK1/2 play an important role in pathological cardiac hypertrophy. The group aims to halt this mechanism and to derive new therapy options from this. Moreover, ERK1/2 also play a role in other severe illnesses such as cancer or arteriosclerosis.

Another approach of the Cardiovascular Pharmacology group is a mechanism that leads to an increased pumping capacity (positive inotropy), but without permanently harming the heart. Such a positive effect is quite unusual for positive inotropes, so that this signalling pathway might be another approach for therapeutic strategies against heart failure.

To uncover these and other regulatory mechanisms in a diseased heart, the group works with purified proteins, cell lines, primary cells, tissues, and different molecular biology and biochemistry methods.

Current Publications

Small extracellular vesicles obtained from hypoxic mesenchymal stromal cells have unique characteristics that promote cerebral angiogenesis, brain remodeling and neurological recovery after focal cerebral ischemia in mice

Basic Research in Cardiology, Vol. 116, Nr. 1, , P. 40
Type: Journal article

Murine models for heart failure: Their creation and applicability to human still require critical and careful considerations

IJC Heart & Vessels, Vol. 34, Nr. 34, , P. 100781
Type: Journal article

"Photo-Rimonabant": Synthesis and Biological Evaluation of Novel Photoswitchable Molecules Derived from Rimonabant Lead to a Highly Selective and Nanomolar " Cis-On" CB 1 R Antagonist

ACS chemical neuroscience, Vol. 12, Nr. 9, , P. 1632–1647
Type: Journal article

Cellular Mechanisms of the Anti-Arrhythmic Effect of Cardiac PDE2 Overexpression

International Journal of Molecular Sciences, Vol. 22, Nr. 9,
Type: Journal article

Sulforaphane exposure impairs contractility and mitochondrial function in three-dimensional engineered heart tissue

Redox biology, Vol. 41, , P. 101951
Type: Journal article

INPP5K and SIL1 associated pathologies with overlapping clinical phenotypes converge through dysregulation of PHGDH

Brain,
Type: Journal article