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

Protein Signature of Human Skin Fibroblasts Allows the Study of the Molecular Etiology of Rare Neurological Diseases

Orphanet journal of rare diseases, Vol. 16,
Type: Journal article

Autosomal recessive variants inTUBGCP2alter theg-tubulin ring complex leading toneurodevelopmental disease

iScience, Vol. 24, Nr. 1, , P. 101948
Type: Journal article

Molecular pathophysiology of human MICU1-deficiency

Neuropathology and applied neurobiology,
Type: Journal article

Metabolic shift underlies recovery in reversible infantile respiratory chain deficiency

The EMBO journal, Vol. 39, Nr. 23,
Type: Journal article

Simple targeted assays for metabolic pathways and signaling: a powerful tool for targeted proteomics

Analytical Chemistry, Vol. 92, Nr. 20, , P. 13672–13676
Type: Journal article

Ca2+ functions as a molecular switch that controls the mutually exclusive complex formation of pyridoxal phosphatase with CIB1 or Calmodulin

FEBS Letters, Vol. 594, Nr. 13, , P. 2099–2115
Type: Journal article