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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.
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Epithelial-mesenchymal transition and its implications for fibrosis

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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

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Figure 2

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Epithelial plasticity can lead to classical EMT (loss of cell-cell and c...
Epithelial plasticity can lead to classical EMT (loss of cell-cell and cell-substratum attachments, new actin rearrangements, and gain of mobility) or reversible scatter, which looks like EMT but is not enduring and can revert. These events are regulated by ligand-inducible intrinsic kinase receptors on the cell surface, which modulate small GTPases, Smads, PI3Ks, MAP kinases, and the availability of β-catenin to coactivate LEF in the nucleus. Free levels of b-catenin are regulated by E-cadherin or APC/β-catenin/Axin complexes, the latter of which shuttle b-catenin between ubiquination or utilization in adherens junctions. Activation of nuclear transcription provides new transcriptional regulators (Snail, SIP1, Ets, and FTS-BP/CarG box binding factor) of the EMT proteome. The EMT proteome comprises proteins listed in Table 1. The variability of receptors, kinases, and the emergence of combined preferences for signaling pathways determine the plasticity unique to each epithelium.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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