Division - Fibrosis

In the Fibrosis Research Unit we aim to understand and overcome the mechanisms that drive pathological tissue remodeling and scarring. Our central focus is the development of a comprehensive Fibrosis Atlas—an integrative resource capturing cellular, molecular, and microenvironmental processes across different organs of one individuum affected by fibrosis. By combining systematic profiling, state of the art spatial technologies with advanced imaging and computational tools, we strive to map fibrosis progression and identify key intervention points.

Fibrosis represents a final common pathway of many chronic diseases, leading to organ dysfunction in the liver, adipose tissue, kidney, heart, and lung. Despite its major clinical impact, effective anti-fibrotic therapies remain limited. The Fibrosis Research Unit investigates how fibroblasts, immune cells, and extracellular matrix signals cooperate to maintain and amplify scarring responses. Our work integrates in vitro models (primary cell cultures, organoids, multiplex competition assays) with in vivo genetic and disease models to uncover conserved and organ-specific drivers of fibrosis in these organs.

To accelerate therapeutic discovery, we are developing synthetic biology–based screening platforms that allow systematic interrogation of signaling pathways and cellular interactions underlying fibrosis. By engineering reporter systems, controllable gene circuits, and high-throughput perturbation assays, we aim to identify and validate candidate targets for anti-fibrotic interventions.

The long-term goal of our research is to translate mechanistic insights into effective treatments. Through the Fibrosis Atlas and our screening platforms, we seek to build a foundation for precision therapies that can halt or even reverse fibrosis across multiple organ systems.