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

Interference with ERK-dimerization at the nucleocytosolic interface targets pathological ERK1/2 signaling without cardiotoxic side-effects

Nature Communications, Vol. 11, Nr. 1,
Type: Journal article

Severe neurodevelopmental disease caused by a homozygous TLK2 variant

European journal of human genetics, Vol. 28, Nr. 3, , P. 383–387
Type: Journal article

The N-termini of GRK2 and GRK3 simulate the stimulating effects of RKIP on β-adrenoceptors

Biochemical and Biophysical Research Communications, Vol. 520, Nr. 2, , P. 327–332
Type: Journal article

Assessing the role of extracellular signal-regulated kinases 1 and 2 in volume overload-induced cardiac remodelling

ESC heart failure, Vol. 6, Nr. 5, , P. 1015–1026
Type: Journal article

Biodegradable Porous Silicon Nanocontainers as an Effective Drug Carrier for Regulation of the Tumor Cell Death Pathways

Acs biomaterials science & engineering, Vol. 5, Nr. 11, , P. 6063–6071
Type: Journal article

Clinical presentation and proteomic signature of patients with TANGO2 mutations

Journal of Inherited Metabolic Disease, Vol. 43, Nr. 2, , P. 297–308
Type: Journal article