We are analyzing https://link.springer.com/article/10.1007/s11926-007-0008-z.

Title:
New developments in fibroblast and myofibroblast biology: Implications for fibrosis and scleroderma | Current Rheumatology Reports
Description:
The concept of mesenchymal fibroblasts has evolved over the past two decades from a relatively inert structural cell type to a dynamic, pluripotent cell lineage controlling normal connective tissue formation, homeostasis, and repair and as principle players in pathogenic scarring and fibrosis. In wound healing and tissue repair, fibroblasts provide proinflammatory signals and synthesize interstitial collagens, fibronectins, and other matrix components to repair the damaged tissue. Fibroblasts can differentiate into the myofibroblast, a specialized contractile cell type responsible for wound closure, tissue contraction, and scarring. This article reviews our current understanding of the origins of mesenchymal cells and their role in excessive scarring and fibrogenesis and in the systemic fibrotic disease scleroderma.
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.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We can't see how the site brings in money.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

article, google, scholar, pubmed, cas, fibroblasts, cell, systemic, fibrosis, cells, sclerosis, growth, fibroblast, scleroderma, tissue, abraham, myofibroblast, clin, arthritis, rheum, mesenchymal, role, stem, biol, factor, transforming, human, sci, invest, rheumatol, proc, expression, pathol, privacy, cookies, content, phd, rajkumar, repair, scarring, wound, disease, skin, natl, acad, gene, shiwen, receptor, essential, publish,

Topics {✒️}

rac/phosphoinositide 3-kinase/akt-dependent pathway platelet-derived growth factor transforming growth factor-beta1 month download article/chapter bone marrow-derived cells diminishes tgf-beta production connective tissue remodelling connective tissue remodeling stem cell factor mesenchymal stem cells pluripotent stem cells tissue engineering references monocyte chemoattractant protein-1 tgf-beta signaling full article pdf terminal cell lineage epithelial-mesenchymal transition epithelial-mesenchymal transformation marrow stromal cells enhanced myofibroblastic differentiation normal tissue repair human dermal fibroblasts privacy choices/manage cookies gene expression signature bochaton-piallat ml tgf-beta1 production vineeth rajkumar msc alveolar epithelial cells mesenchymal cells related subjects endogenous il-1alpha elevated serum levels il-6-deficient mice enhanced contractile phenotype shi-wen human skin fibroblasts il-13alpha2 receptor collagen-secreting cells collagen-producing cells tight-skin mutation cutaneous scleroderma fibroblasts endothelin receptor antagonists keratinocyte-fibroblast cocultures european economic area synthesize interstitial collagens fibronectin domain ed postlethwaite ae peripheral blood excessive dermal scarring university college london

Questions {❓}

Korn JH: What’s wrong with the scleroderma fibroblast?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:New developments in fibroblast and myofibroblast biology: Implications for fibrosis and scleroderma
         description:The concept of mesenchymal fibroblasts has evolved over the past two decades from a relatively inert structural cell type to a dynamic, pluripotent cell lineage controlling normal connective tissue formation, homeostasis, and repair and as principle players in pathogenic scarring and fibrosis. In wound healing and tissue repair, fibroblasts provide proinflammatory signals and synthesize interstitial collagens, fibronectins, and other matrix components to repair the damaged tissue. Fibroblasts can differentiate into the myofibroblast, a specialized contractile cell type responsible for wound closure, tissue contraction, and scarring. This article reviews our current understanding of the origins of mesenchymal cells and their role in excessive scarring and fibrogenesis and in the systemic fibrotic disease scleroderma.
         datePublished:2007-06-03T00:00:00Z
         dateModified:2007-06-03T00:00:00Z
         pageStart:136
         pageEnd:143
         sameAs:https://doi.org/10.1007/s11926-007-0008-z
         keywords:
            Scleroderma
            Systemic Sclerosis
            Connective Tissue Growth Factor
            Cartilage Oligomeric Matrix Protein
            Mesenchymal Cell Population
            Rheumatology
         image:
         isPartOf:
            name:Current Rheumatology Reports
            issn:
               1534-6307
               1523-3774
            volumeNumber:9
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Current Science Inc.
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:David J. Abraham
               affiliation:
                     name:University College London (Hampstead Campus)
                     address:
                        name:Centre for Rheumatology, Department of Medicine, Royal Free and University College Medical School, University College London (Hampstead Campus), London, UK
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Beate Eckes
               type:Person
               name:Vineeth Rajkumar
               type:Person
               name:Thomas Krieg
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:New developments in fibroblast and myofibroblast biology: Implications for fibrosis and scleroderma
      description:The concept of mesenchymal fibroblasts has evolved over the past two decades from a relatively inert structural cell type to a dynamic, pluripotent cell lineage controlling normal connective tissue formation, homeostasis, and repair and as principle players in pathogenic scarring and fibrosis. In wound healing and tissue repair, fibroblasts provide proinflammatory signals and synthesize interstitial collagens, fibronectins, and other matrix components to repair the damaged tissue. Fibroblasts can differentiate into the myofibroblast, a specialized contractile cell type responsible for wound closure, tissue contraction, and scarring. This article reviews our current understanding of the origins of mesenchymal cells and their role in excessive scarring and fibrogenesis and in the systemic fibrotic disease scleroderma.
      datePublished:2007-06-03T00:00:00Z
      dateModified:2007-06-03T00:00:00Z
      pageStart:136
      pageEnd:143
      sameAs:https://doi.org/10.1007/s11926-007-0008-z
      keywords:
         Scleroderma
         Systemic Sclerosis
         Connective Tissue Growth Factor
         Cartilage Oligomeric Matrix Protein
         Mesenchymal Cell Population
         Rheumatology
      image:
      isPartOf:
         name:Current Rheumatology Reports
         issn:
            1534-6307
            1523-3774
         volumeNumber:9
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Current Science Inc.
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:David J. Abraham
            affiliation:
                  name:University College London (Hampstead Campus)
                  address:
                     name:Centre for Rheumatology, Department of Medicine, Royal Free and University College Medical School, University College London (Hampstead Campus), London, UK
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Beate Eckes
            type:Person
            name:Vineeth Rajkumar
            type:Person
            name:Thomas Krieg
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Current Rheumatology Reports
      issn:
         1534-6307
         1523-3774
      volumeNumber:9
Organization:
      name:Current Science Inc.
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University College London (Hampstead Campus)
      address:
         name:Centre for Rheumatology, Department of Medicine, Royal Free and University College Medical School, University College London (Hampstead Campus), London, UK
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:David J. Abraham
      affiliation:
            name:University College London (Hampstead Campus)
            address:
               name:Centre for Rheumatology, Department of Medicine, Royal Free and University College Medical School, University College London (Hampstead Campus), London, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Beate Eckes
      name:Vineeth Rajkumar
      name:Thomas Krieg
PostalAddress:
      name:Centre for Rheumatology, Department of Medicine, Royal Free and University College Medical School, University College London (Hampstead Campus), London, UK
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(195)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

4.01s.

LINK . SPRINGER . COM {}