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We mapped fibroblast to myofibroblast differentiation in this process and identified notable changes in the cardiac vasculature, suggesting inflammation and dysfunction. An integrated analysis of cardiac cellular responses to uremic toxins pointed toward endothelin-1 and methylglyoxal being involved in capillary dysfunction and TNF\u03b1 driving cardiomyocyte hypertrophy in CKD, which was validated in vitro and in vivo. TNF\u03b1 inhibition in vivo ameliorated the cardiac phenotype in CKD. Thus, interventional approaches directed against uremic toxins, such as TNF\u03b1, hold promise to ameliorate cardiac remodeling in CKD.<\/jats:p>","DOI":"10.1126\/sciadv.adj4846","type":"journal-article","created":{"date-parts":[[2023,11,24]],"date-time":"2023-11-24T18:58:15Z","timestamp":1700852295000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":24,"title":["Mapping cardiac remodeling in chronic kidney disease"],"prefix":"10.1126","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8097-7660","authenticated-orcid":true,"given":"Nadine","family":"Kaesler","sequence":"first","affiliation":[{"name":"Clinic for Renal and Hypertensive Disorders, Rheumatological and Immunological Disease, University Hospital of the RWTH Aachen, Aachen, Germany."},{"name":"Institute of Experimental Medicine and Systems Biology, University Hospital of the RWTH Aachen, Aachen, 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