Chronic kidney disease promotes structural changes within the heart that increase the risk for a cardiovascular event dramatically. Often, these patients suffer from heart disease and die from sudden heart failure. Scientists from the Medical Clinic II, in charge of Dr. Nadine Kaesler and Prof. Kramann, in collaboration with the Institute of Computational Genomics (Mingbo Cheng and Prof. Costa), now succeeded to reconstruct the characteristic cardiac remodeling in a mouse model, focusing on an increase in cardiac size, enrichment of connective tissue and capillary changes. By combining state of the art biotechnological and bioinformatics methods, the underlining pathological mechanisms up to single factors were identified. In addition, some findings were confirmed in human tissues and human cell culture models. Especially, a role of pro-inflammatory actions via TNFα, the JAK-STAT pathway, as well as roles of the uremic toxins endothelin-1 and methylglyoxal, which accumulate in chronic kidney disease, were highlighted. Now, more targeted therapeutically approaches can be developed to stop the pathological remodeling. The study was published in the scientific journal Science Advances:
DOI: 10.1126/sciadv.adj4846 http://www.science.org/doi/10.1126/sciadv.adj4846
