For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
437
views
89
references
 Top references
cited by
235
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    2
    shares
      619
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Inflammation and EMT: an alliance towards organ fibrosis and cancer progression

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Recent advances in our understanding of the molecular pathways that govern the association of inflammation with organ fibrosis and cancer point to the epithelial to mesenchymal transition (EMT) as the common link in the progression of these devastating diseases. The EMT is a crucial process in the development of different tissues in the embryo and its reactivation in the adult may be regarded as a physiological attempt to control inflammatory responses and to ‘heal’ damaged tissue. However, in pathological contexts such as in tumours or during the development of organ fibrosis, this healing response adopts a sinister nature, steering these diseases towards metastasis and organ failure. Importantly, the chronic inflammatory microenvironment common to fibrotic and cancer cells emerges as a decisive factor in the induction of the pathological EMT.

          Related collections

          Most cited references89

          • Record: found
          • Abstract: found
          • Article: not found

          Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

          M Shull, I Ormsby, A Kier … (1992)
          Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.
          Article 0 comments Cited 482 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            NF-kappaB activation by reactive oxygen species: fifteen years later.

            Geoffrey Gloire, Sylvie Legrand-Poels, Jacques Piette (2006)
            The transcription factor NF-kappaB plays a major role in coordinating innate and adaptative immunity, cellular proliferation, apoptosis and development. Since the discovery in 1991 that NF-kappaB may be activated by H(2)O(2), several laboratories have put a considerable effort into dissecting the molecular mechanisms underlying this activation. Whereas early studies revealed an atypical mechanism of activation, leading to IkappaBalpha Y42 phosphorylation independently of IkappaB kinase (IKK), recent findings suggest that H(2)O(2) activates NF-kappaB mainly through the classical IKK-dependent pathway. The molecular mechanisms leading to IKK activation are, however, cell-type specific and will be presented here. In this review, we also describe the effect of other ROS (HOCl and (1)O(2)) and reactive nitrogen species on NF-kappaB activation. Finally, we critically review the recent data highlighting the role of ROS in NF-kappaB activation by proinflammatory cytokines (TNF-alpha and IL-1beta) and lipopolysaccharide (LPS), two major components of innate immunity.
            Article 0 comments Cited 378 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              BMP-7 counteracts TGF-beta1-induced epithelial-to-mesenchymal transition and reverses chronic renal injury.

              Michael Zeisberg, Jun-ichi Hanai, Hikaru Sugimoto … (2003)
              Bone morphogenic protein (BMP)-7 is a 35-kDa homodimeric protein and a member of the transforming growth factor (TGF)-beta superfamily. BMP-7 expression is highest in the kidney, and its genetic deletion in mice leads to severe impairment of eye, skeletal and kidney development. Here we report that BMP-7 reverses TGF-beta1-induced epithelial-to-mesenchymal transition (EMT) by reinduction of E-cadherin, a key epithelial cell adhesion molecule. Additionally, we provide molecular evidence for Smad-dependent reversal of TGF-beta1-induced EMT by BMP-7 in renal tubular epithelial cells and mammary ductal epithelial cells. In the kidney, EMT-induced accumulation of myofibroblasts and subsequent tubular atrophy are considered key determinants of renal fibrosis during chronic renal injury. We therefore tested the potential of BMP-7 to reverse TGF-beta1-induced de novo EMT in a mouse model of chronic renal injury. Our results show that systemic administration of recombinant human BMP-7 leads to repair of severely damaged renal tubular epithelial cells, in association with reversal of chronic renal injury. Collectively, these results provide evidence of cross talk between BMP-7 and TGF-beta1 in the regulation of EMT in health and disease.
              Article 0 comments Cited 329 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): EMBO Mol Med
                Journal ID (iso-abbrev): EMBO Mol Med
                Journal ID (publisher-id): emmm
                Title: EMBO Molecular Medicine
                Publisher: WILEY-VCH Verlag (Weinheim )
                ISSN (Print): 1757-4676
                ISSN (Electronic): 1757-4684
                Publication date (Print): September 2009
                Volume: 1
                Issue: 6-7
                Pages: 303-314
                Affiliations
                [1 ]simpleDepartamento de Fisiología y Farmacología, Universidad de Salamanca, Edificio Departamental, Campus Miguel de Unamuno Salamanca, Spain
                [2 ]simpleInstituto de Neurociencias CSIC-UMH San Juan de Alicante, Spain
                Author notes
                * Corresponding author: Tel: (+34) 965 919243; Fax: (+34) 965 919561; E-mail: anieto@ 123456umh.es
                Article
                DOI: 10.1002/emmm.200900043
                PMC ID: 3378143
                PubMed ID: 20049734
                SO-VID: cc36662e-9972-4199-8281-d9d1d2102107
                Copyright © Copyright © 2009 EMBO Molecular Medicine
                History
                Date received : 18 June 2009
                Date revision received : 17 August 2009
                Date accepted : 26 August 2009
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: epithelial–mesenchymal transition,tnf-α,inflammation,tgf-β,nf-κb
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: epithelial–mesenchymal transition, tnf-α, inflammation, tgf-β, nf-κb

                Comments

                Comment on this article

                scite_

                Similar content619

                See all similar

                Cited by231

                See all cited by

                Most referenced authors2,238

                See all reference authors