Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Immune Environment in Glioblastoma (Feb 2023)
    • Korsmeyer Award 25th Anniversary Collection (Jan 2023)
    • Aging (Jul 2022)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Research letters
    • Letters to the editor
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Research letters
  • Letters to the editor
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Epithelial-mesenchymal transition and its implications for fibrosis
Raghu Kalluri, Eric G. Neilson
Raghu Kalluri, Eric G. Neilson
Published December 15, 2003
Citation Information: J Clin Invest. 2003;112(12):1776-1784. https://doi.org/10.1172/JCI20530.
View: Text | PDF
Spotlight

Epithelial-mesenchymal transition and its implications for fibrosis

  • Text
  • PDF
Abstract

Epithelial to mesenchymal transition (EMT) is a central mechanism for diversifying the cells found in complex tissues. This dynamic process helps organize the formation of the body plan, and while EMT is well studied in the context of embryonic development, it also plays a role in the genesis of fibroblasts during organ fibrosis in adult tissues. Emerging evidence from studies of renal fibrosis suggests that more than a third of all disease-related fibroblasts originate from tubular epithelia at the site of injury. This review highlights recent advances in the process of EMT signaling in health and disease and how it may be attenuated or reversed by selective cytokines and growth factors.

Authors

Raghu Kalluri, Eric G. Neilson

×

Figure 3

Options: View larger image (or click on image) Download as PowerPoint
Origin of fibroblasts during kidney fibrosis. (a) Fibrotic kidney which ...
Origin of fibroblasts during kidney fibrosis. (a) Fibrotic kidney which displays accumulation of numerous fibroblasts (blue arrow), damaged kidney tubules (yellow arrow), and blood vessels (green arrow). (b) Normal kidney with proper tubular structures and very few fibroblasts. (c) Schematic illustration of three possible mechanisms via which fibroblasts can originate during kidney injury. Recent experiments suggest that approximately 14–15% of fibroblasts are from bone marrow, 36% can arise via local EMT involving tubular epithelial cells under inflammatory stress, and the rest are likely contributed by proliferation of fibroblasts from all sources. (d) Systemic treatment of mice with renal fibrosis using recombinant human BMP-7 results in reversal of renal disease due to severe decrease in EMT-derived fibroblasts and potentially bone marrow–derived fibroblasts. Such events likely have a cascade of beneficial effects that decreasing the overall number of fibroblasts in the kidney, and attenuating fibrosis.

Copyright © 2023 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts