Many of the phenotypes in human kidney disease are only detectable at the ultrastructural level. This holds also true for the model systems of genetic and epigenetic based disturbances of renal development, biology or aging. Our group applies transmission and scanning microscope techniques in human and animal tissue (e.g. mouse, rat, zebrafish, drosophila) in order to detect and characterize subtle ultrastructural alterations e.g. of the glomerular filtration barrier, the actin cytoskeleton or intracellular vesicle formation and trafficking at a qualitative and quantitative level.

Moreover, our thematic focus deals with the understanding of mechanisms underlying kidney aging an issue of growing relevance in the aging population of western countries. To this end we make use of the progeroid Ercc1Δ/- mutant mouse line as an experimental platform for studies into aging. It harbors attenuated Excision repair cross-complementation 1 activity, a key component of several DNA repair pathways. In this model system we apply different conditions which we and others have recently shown to have beneficial effects on aging like modulation of the activin/myostatin pathway or dietary restriction. By deep morphological, functional and molecular (single nuclei transcriptomics) analysis we aim to identify pathways involved in aging in different cell types of the kidney and in other organs like muscle, liver or CNS. Finally, we have a special interest in the concept of inter-organ communication during aging that is now emerging. We hope to identify kidney derived factors influencing the aging of other organ systems and vice versa.