Stem Cells International

Stem Cells International / 2016 / Article
Special Issue

Mesenchymal Transitions in Development and Disease

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Editorial | Open Access

Volume 2016 |Article ID 5107517 |

Damian Medici, Pura Muñoz-Cánoves, Pan-Chyr Yang, Silvia Brunelli, "Mesenchymal Transitions in Development and Disease", Stem Cells International, vol. 2016, Article ID 5107517, 2 pages, 2016.

Mesenchymal Transitions in Development and Disease

Received14 Mar 2016
Accepted14 Mar 2016
Published02 Aug 2016

The ability of epithelial cells and endothelial cells to transform into mesenchymal cells is one of the most basic cellular mechanisms in biology. This process, referred to as epithelial-mesenchymal transition (EMT) or endothelial-mesenchymal transition (EndMT), regulates various stages of embryonic development and contributes to the progression of a wide array of diseases and in tissue repair [1, 2].

During embryogenesis, EMT is essential for gastrulation, primitive streak formation, somite dissociation, neural crest development, and palate and lip fusion [3]. EndMT is critical for cardiac development, particularly in the formation of the valves and septa of the heart [4] and the generation of mesodermal cells and multipotent progenitors [5].

In the adult organism, EMT and EndMT are usually dormant until pathological stimuli awaken this embryonic mechanism. For example, EMT is the primary mechanism of cancer metastasis [6, 7], whereas EndMT forms cancer-associated fibroblasts in the tumor microenvironment [8]. Also, both EMT and EndMT have been shown to generate fibroblasts that cause the formation of scar tissue after tissue injury or in association with inflammatory and fibrotic diseases [911].

Mesenchymal transitions have traditionally been considered to have a positive effect in development and a negative effect in disease. However, novel findings regarding the stem cell phenotype generated by EMT and EndMT [12, 13] suggest that they may have therapeutic potential for the treatment of various degenerative diseases. This marks an exciting period in this field of research, which may provide new methods for tissue engineering and regeneration by harnessing the power of this embryonic mechanism.

In this special issue, the articles focus on the cutting-edge research on EMT/EndMT, including the role of this mechanism in regenerative medicine, peritoneal fibrosis, liver fibrosis, systemic sclerosis, and angiogenesis. This issue also explores how factors such as mechanical force, vitamin D signaling, and noncoding RNAs regulate mesenchymal transitions, which may provide novel insight into future avenues of research and therapeutic development.

Damian Medici
Pura Muñoz-Cánoves
Pan-Chyr Yang
Silvia Brunelli


  1. J. P. Thiery, H. Acloque, R. Y. J. Huang, and M. A. Nieto, “Epithelial-mesenchymal transitions in development and disease,” Cell, vol. 139, no. 5, pp. 871–890, 2009. View at: Publisher Site | Google Scholar
  2. R. Kalluri and R. A. Weinberg, “The basics of epithelial-mesenchymal transition,” The Journal of Clinical Investigation, vol. 119, no. 6, pp. 1420–1428, 2009. View at: Publisher Site | Google Scholar
  3. E. D. Hay, “The mesenchymal cell, its role in the embryo, and the remarkable signaling mechanisms that create it,” Developmental Dynamics, vol. 233, no. 3, pp. 706–720, 2005. View at: Publisher Site | Google Scholar
  4. J. C. Kovacic, N. Mercader, M. Torres, M. Boehm, and V. Fuster, “Epithelial-to-mesenchymal and endothelial-to-mesenchymal transition from cardiovascular development to disease,” Circulation, vol. 125, no. 14, pp. 1795–1808, 2012. View at: Publisher Site | Google Scholar
  5. E. Azzoni, V. Conti, L. Campana et al., “Hemogenic endothelium generates mesoangioblasts that contribute to several mesodermal lineages in vivo,” Development, vol. 141, no. 9, pp. 1821–1834, 2014. View at: Publisher Site | Google Scholar
  6. G. P. Gupta and J. Massagué, “Cancer metastasis: building a framework,” Cell, vol. 127, no. 4, pp. 679–695, 2006. View at: Publisher Site | Google Scholar
  7. J.-Y. Shih and P.-C. Yang, “The EMT regulator slug and lung carcinogenesis,” Carcinogenesis, vol. 32, no. 9, pp. 1299–1304, 2011. View at: Publisher Site | Google Scholar
  8. S. Potenta, E. Zeisberg, and R. Kalluri, “The role of endothelial-to-mesenchymal transition in cancer progression,” British Journal of Cancer, vol. 99, no. 9, pp. 1375–1379, 2008. View at: Publisher Site | Google Scholar
  9. R. Kalluri and E. G. Neilson, “Epithelial-mesenchymal transition and its implications for fibrosis,” The Journal of Clinical Investigation, vol. 112, no. 12, pp. 1776–1784, 2003. View at: Publisher Site | Google Scholar
  10. S. Piera-Velazquez, Z. Li, and S. A. Jimenez, “Role of endothelial-mesenchymal transition (EndoMT) in the pathogenesis of fibrotic disorders,” The American Journal of Pathology, vol. 179, no. 3, pp. 1074–1080, 2011. View at: Publisher Site | Google Scholar
  11. P. Pessina, Y. Kharraz, M. Jardí et al., “Fibrogenic cell plasticity blunts tissue regeneration and aggravates muscular dystrophy,” Stem Cell Reports, vol. 4, no. 6, pp. 1046–1060, 2015. View at: Publisher Site | Google Scholar
  12. C. Scheel and R. A. Weinberg, “Cancer stem cells and epithelial-mesenchymal transition: concepts and molecular links,” Seminars in Cancer Biology, vol. 22, no. 5-6, pp. 396–403, 2012. View at: Publisher Site | Google Scholar
  13. D. Medici and R. Kalluri, “Endothelial-mesenchymal transition and its contribution to the emergence of stem cell phenotype,” Seminars in Cancer Biology, vol. 22, no. 5-6, pp. 379–384, 2012. View at: Publisher Site | Google Scholar

Copyright © 2016 Damian Medici et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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