Header Navigation

Extracellular vesicles (EVs) are small membrane bound spheres, released by almost all cells of the body, that have been identified as critical contributors to cancer cell biology as well as immune and metabolic signaling. Membranous Nephropathy (MN) is a major cause of proteinuric kidney disease and the need for renal replacement therapy. It is caused by damage to the epithelial cells of the kidney filtration unit, podocytes. We aim to characterize the podocyte-specific release and cargo of EVs and identify alterations in MN.

While degeneration of the articular cartilage is the main feature of osteoarthritis (OA), complex mechanisms influence its development and progression. In this regard, a special role is attributed to the bone below the cartilage (so-called subchondral bone). We are performing a comprehensive imaging and biomechanical analysis of the subchondral bone of human samples with different grades of OA severity. The aim of the project is to decipher the cellular, bone quality and biochemical changes with identification of stage-specific and topographic patterns.

High blood pressure, diabetes, smoking and lipid metabolism disorders are risk factors for the development of cardiovascular diseases (CVD) which result in heart attacks and stroke, the main causes of morbidity and mortality worldwide. Vascular dysfunction represents an early and decisive step in the development of CVD that cannot be adequately addressed with current therapies.

Therapeutic strategies against cancer that activate the body's own immune system and thus kill cancer cells have been implemented successfully for patients with bladder cancer. However, predicting which patients will benefit from this type of therapy is only possible to a limited extent. Earlier studies showed that novel tissue markers, including inflammation markers and viral elements that have been integrated into the human genome for thousands of years (so-called endogenous retroviruses), can predict the success of immunotherapies.

Pulmonary fibrosis (PF) is a lethal, progressive lung disorder affecting millions of patients worldwide, with limited therapeutic options. Inflammatory infiltration and fibroblast-to-myofibroblast activation leading to excessive extracellular matrix deposition underlie the pathogenesis of PF. While pathways promoting these cellular alterations have been described, endogenous factors counter-regulating such changes are barely known.