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

Trends Endocrinol Metab. 2016 Oct;27(10):681-695. doi: 10.1016/j.tem.2016.06.004. Epub 2016 Jun 29.

Abstract

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.

Keywords: acute kidney injury; chronic kidney disease; epithelial-to-mesenchymal transition; kidney fibrosis; myofibroblasts.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / metabolism
  • Acute Kidney Injury / pathology
  • Animals
  • Disease Progression
  • Epithelial-Mesenchymal Transition / genetics
  • Epithelial-Mesenchymal Transition / physiology*
  • Fibrosis / metabolism*
  • Fibrosis / pathology*
  • Humans
  • Kidney Diseases / metabolism*
  • Kidney Diseases / pathology*
  • Myofibroblasts / metabolism
  • Signal Transduction / genetics
  • Signal Transduction / physiology