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J Clin Med. 2018 Jan 30;7(2). doi: 10.3390/jcm7020015.

CERA Attenuates Kidney Fibrogenesis in the db/db Mouse by Influencing the Renal Myofibroblast Generation.

Journal of clinical medicine

Christin Fischer, Natalie Deininger, Gunter Wolf, Ivonne Loeffler

Affiliations

  1. Department of Internal Medicine III, University Hospital Jena, Am Klinikum 1, D-07747 Jena, Germany. [email protected].
  2. Institute of Medical Genetics and Applied Genomics, University Tübingen, Calwerstraße 7, D-72076 Tübingen, Germany. [email protected].
  3. Department of Internal Medicine III, University Hospital Jena, Am Klinikum 1, D-07747 Jena, Germany. [email protected].
  4. Department of Internal Medicine III, University Hospital Jena, Am Klinikum 1, D-07747 Jena, Germany. [email protected].

PMID: 29385703 PMCID: PMC5852431 DOI: 10.3390/jcm7020015

Abstract

Tubulointerstitial fibrosis (TIF) is a pivotal pathophysiological process in patients with diabetic nephropathy (DN). Multiple profibrotic factors and cell types, including transforming growth factor beta 1 (TGF-β1) and interstitial myofibroblasts, respectively, are responsible for the accumulation of extracellular matrix in the kidney. Matrix-producing myofibroblasts can originate from different sources and different mechanisms are involved in the activation process of the myofibroblasts in the fibrotic kidney. In this study, 16-week-old

Keywords: CERA; DN; EPO; TIF; db/db mouse; diabetic nephropathy; erythropoietin; myofibroblast; tubulointerstitial fibrosis; type 2 diabetes

Conflict of interest statement

The authors declare no conflict of interest.

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