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Partial Epithelial-to-Mesenchymal Transition and Other New Mechanisms of Kidney Fibrosis

Journal

TRENDS IN ENDOCRINOLOGY AND METABOLISM
Volume 27, Issue 10, Pages 681-695

Publisher

ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2016.06.004

Keywords

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Funding

  1. Deutsche Forschungsgemeinschaft [ZE523/2-1, ZE523/4-1]
  2. Cancer Prevention and Research Institute of Texas
  3. MD Anderson Cancer Center

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Kidney fibrosis is the unavoidable consequence of chronic kidney disease irrespective of the primary underlying insult. It is a complex phenomenon governed by the interplay between different cellular components and intricate networks of signaling pathways, which together lead to loss of renal functionality and replacement of kidney parenchyma with scar tissue. An immense effort has recently been made to understand the molecular and cellular mechanisms leading to kidney fibrosis. The cellular protagonists of this process include myofibroblasts, tubular epithelial cells, endothelial cells, and immune cells. We discuss here the most recent findings, including partial epithelial-to-mesenchymal transition (EMT), in the initiation and progression of tissue fibrosis and chronic kidney disease (CKD). A deep understanding of these mechanisms will allow the development of effective therapies.

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