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Nadine Tuechler, Muzamil M Khan, Martin Garrido-Rodriguez, Mira Lea Burtscher, Denes Turei, Rafael Kramann, Susanne Delecluse, Christoph A. Merten, Julio Saez-Rodriguez, Rainer Pepperkok (EMBL Heidelberg, Meyerhofstraße 1, 69117 Heidelberg)
Organ fibrosis is the main driver of Chronic kidney disease (CKD), which is excessive accumulation of extracellular matrix (ECM). Myofibroblasts are the cellular correlate of disease progression. The underlying processes of these cells, like ECM production, are driven by the master regulator TGF-β. Despite progresses in understanding the disease, there are no treatments available, and current diagnostic indicators neither facilitate early detection of CKD, nor correlate with actual renal damage. Thus, we aim to provide mechanistic insights into CKD progression by using human kidney-derived myofibroblasts. Our goal is to model how these cells contribute to fibrosis by studying their kinetic response to TGF-β. We apply multi-omics readouts coupled with quantitative imaging of the ECM. Our data revealed well-known mechanisms and novel factors that are now suspect to experimental validation to explore their potential as fibrotic disease markers. Using mechanistic modeling and integration of multiple datasets, we aim to provide a better understanding of factors and mechanisms driving kidney fibrosis and eventually markers and drug targets that can be taken further into clinical studies.