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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries

We are analyzing https://link.springer.com/article/10.1007/s00109-003-0517-9.

Title:
The role of epithelial-to-mesenchymal transition in renal fibrosis | Journal of Molecular Medicine
Description:
Epithelial-to-mesenchymal transition (EMT) involving injured epithelial cells plays an important role in the progression of fibrosis in the kidney. Tubular epithelial cells can acquire a mesenchymal phenotype, and enhanced migratory capacity enabling them to transit from the renal tubular microenvironment into the interstitial space and escape potential apoptotic cell death. EMT is a major contributor to the pathogenesis of renal fibrosis, as it leads to a substantial increase in the number of myofibroblasts, leading to tubular atrophy. However, recent findings suggest that EMT involving tubular epithelial cell is a reversible process, potentially determined by the surviving cells to facilitate the repopulation of injured tubules with new functional epithelia. Major regulators of renal epithelial cell plasticity in the kidney are two multifunctional growth factors, bone morphogenic protein-7 (BMP-7) and transforming growth factor β1 (TGF-β1). While TGF-β1 is a well-established inducer of EMT involving renal tubular epithelial cells, BMP-7 reverses EMT by directly counteracting TGF-β-induced Smad-dependent cell signaling in renal tubular epithelial cells. Such antagonism results in the repair of injured kidneys, suggesting that modulation of epithelial cell plasticity has therapeutic advantages.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We don't see any clear sign of profit-making.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

google, scholar, pubmed, cas, article, cell, renal, epithelial, fibrosis, growth, protein, cells, kidney, transition, kalluri, tubular, bone, transforming, tgfbeta, zeisberg, bmp, factor, epithelialmesenchymal, physiol, biol, development, nat, int, expression, role, epithelialtomesenchymal, emt, mesenchymal, signaling, med, neilson, strutz, mol, morphogenetic, morphogenic, matrix, transdifferentiation, dev, nature, usa, ecadherin, center, privacy, cookies, content,

Topics {✒️}

beta-catenin/lef-1 signaling pathway transforming growth factor-beta month download article/chapter tgf-beta induced transdifferentiation transcription factor snail tgf-beta/bmp signaling multiple tgf-beta signals tubular epithelial-myofibroblast transdifferentiation repressing e-cadherin expression bone morphogenic protein-7 epithelial-mesenchymal transitions epithelial-mesenchymal transition renal branching morphogenesis e-cadherin gene expression renal tubular microenvironment tgf-beta signaling chronic renal fibrosis epithelial-mesenchymal transformation renal interstitial fibrosis bone morphogenetic protein-7 multifunctional growth factors receptor/alk-5 full article pdf epithelial mesenchymal interactions high affinity binding epithelial-myofibroblast transdifferentiation epithelio-mesenchymal transformation targeting tgf-beta tgf-beta signalling tgf-beta superfamily tgf-beta family tgf-beta responses tubular epithelial cells raghu kalluri e-cadherin expression human renal biopsies privacy choices/manage cookies bone morphogenetic proteins embryonic renal epithelia renal disease cadherin-catenin system experimental kidney disease article zeisberg bmp-2/4 signaling mediated epithelial cell plasticity mammary epithelial cells epithelial tumour cells author information authors harvard medical school progressive tubulointerstitial fibrosis

Questions {❓}

  • Herzlinger D (2002) Renal interstitial fibrosis: remembrance of things past?

Schema {🗺️}

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         headline:The role of epithelial-to-mesenchymal transition in renal fibrosis
         description:Epithelial-to-mesenchymal transition (EMT) involving injured epithelial cells plays an important role in the progression of fibrosis in the kidney. Tubular epithelial cells can acquire a mesenchymal phenotype, and enhanced migratory capacity enabling them to transit from the renal tubular microenvironment into the interstitial space and escape potential apoptotic cell death. EMT is a major contributor to the pathogenesis of renal fibrosis, as it leads to a substantial increase in the number of myofibroblasts, leading to tubular atrophy. However, recent findings suggest that EMT involving tubular epithelial cell is a reversible process, potentially determined by the surviving cells to facilitate the repopulation of injured tubules with new functional epithelia. Major regulators of renal epithelial cell plasticity in the kidney are two multifunctional growth factors, bone morphogenic protein-7 (BMP-7) and transforming growth factor β1 (TGF-β1). While TGF-β1 is a well-established inducer of EMT involving renal tubular epithelial cells, BMP-7 reverses EMT by directly counteracting TGF-β-induced Smad-dependent cell signaling in renal tubular epithelial cells. Such antagonism results in the repair of injured kidneys, suggesting that modulation of epithelial cell plasticity has therapeutic advantages.
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            Molecular Medicine
            Human Genetics
            Internal Medicine
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      description:Epithelial-to-mesenchymal transition (EMT) involving injured epithelial cells plays an important role in the progression of fibrosis in the kidney. Tubular epithelial cells can acquire a mesenchymal phenotype, and enhanced migratory capacity enabling them to transit from the renal tubular microenvironment into the interstitial space and escape potential apoptotic cell death. EMT is a major contributor to the pathogenesis of renal fibrosis, as it leads to a substantial increase in the number of myofibroblasts, leading to tubular atrophy. However, recent findings suggest that EMT involving tubular epithelial cell is a reversible process, potentially determined by the surviving cells to facilitate the repopulation of injured tubules with new functional epithelia. Major regulators of renal epithelial cell plasticity in the kidney are two multifunctional growth factors, bone morphogenic protein-7 (BMP-7) and transforming growth factor β1 (TGF-β1). While TGF-β1 is a well-established inducer of EMT involving renal tubular epithelial cells, BMP-7 reverses EMT by directly counteracting TGF-β-induced Smad-dependent cell signaling in renal tubular epithelial cells. Such antagonism results in the repair of injured kidneys, suggesting that modulation of epithelial cell plasticity has therapeutic advantages.
      datePublished:2004-01-30T00:00:00Z
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         Internal Medicine
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External Links {🔗}(232)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

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