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1. Role of the mineralocorticoid receptor in inflammatory cells
Recent data suggest that the mineralocorticoid receptor is expressed in inflammatory cells and exerts proinflammatory effects. We examine its role in cells of the innate and adaptive immune systems in the context of hypertension and infectious disease. We hypothesize that receptor knockout may have beneficial effects in hypertension but emphasize the need to carefully evaluate potential detrimental effects in infectious disease.
2. Role of complement in hypertension and renal disease
The binding of the anaphylatoxins C3a and C5a to their respective receptors—C3aR, C5aR1, and C5aR2—triggers potent proinflammatory signaling. We investigate their contribution to the pathogenesis of hypertension and glomerulonephritis.
3. Role of complement in Takotsubo myocarditis
This disease, also known as “broken heart disease” occurs predominantly in women. Our data suggest that complement receptors play a key role in the pathogenesis of cardiac inflammation and fibrosis. We investigate this using a murine model of isoprenaline-induced myocarditis. In this model, mice develop a reduced ejection fraction during the early phase, followed by inflammation and fibrosis in the later phase.
4. Pathogenesis of so called malignant nephrosclerosis
The pathogenesis of renal injury in so-called malignant nephrosclerosis remains poorly understood. This condition represents a form of thrombotic microangiopathy, characterized by progressive narrowing of interlobular arteries and afferent arterioles, accompanied by intimal fibrosis and a characteristic onion-skin pattern of scarring. Due to the lack of suitable preclinical models, current research relies entirely on human material, including kidney biopsies, induced pluripotent stem cells (iPSCs), and renal organoids.