We are analyzing https://link.springer.com/article/10.1007/s10620-014-3167-6.

Title:
Caspase 3 Inactivation Protects Against Hepatic Cell Death and Ameliorates Fibrogenesis in a Diet-Induced NASH Model | Digestive Diseases and Sciences
Description:
Background/Aims Hepatocyte cell death is a key feature of nonalcoholic steatohepatitis (NASH). As the contribution of specific caspases remains unclear, our aim was to ascertain the effect of caspase 3 suppression on liver injury and fibrogenesis. Methods C57BL/6 wild-type (WT) and caspase 3 knock out (Casp3 −/−) mice were placed on a methionine- and choline-deficient (MCD) diet for 6 weeks to induce steatohepatitis and liver fibrosis. Thereafter, liver injury, liver fibrosis and hepatocellular apoptosis were quantified in liver sections. Additionally, expression of proteins associated with liver inflammation and fibrogenesis was analyzed. Results WT mice fed MCD diet showed marked activation of caspase 3 in hepatocytes, in conjunction with steatohepatitis and increased hepatic triglyceride levels, hepatocyte ballooning, inflammation and fibrosis. Casp3 −/− mice fed the MCD diet showed similar serum aminotransferase levels and NAFLD activity scores (NAS) compared with WT MCD-fed mice. However, Casp3 −/− mice on the MCD diet showed a marked reduction in expression of transcripts for profibrogenic genes, which translated into reduced hepatic collagen deposition. These changes were associated with decreased levels of apoptosis, and a significant reduction in the expression of cytokines involved in inflammatory signaling. Casp3 −/− mice on the MCD showed a reduction in expression of chemokine receptor 2 (CCR2) leading to ameliorated infiltration of inflammatory lymphocyte antigen 6 complex, locus C1 (Ly6c) positive monocytes. Conclusion These findings support a prominent role for hepatocyte caspase 3 activation in NASH-related apoptosis, fibrogenesis and fibrosis which in part is mediated via CCR2-dependent infiltration of Ly6c positive monocytes.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Health & Fitness
Fitness & Wellness

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 tell how the site generates income.

Some websites aren't about earning revenue; they're built to connect communities or raise awareness. There are numerous motivations behind creating websites. This might be one of them. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

article, pubmed, google, scholar, liver, cas, nonalcoholic, hepatic, steatohepatitis, feldstein, apoptosis, disease, fatty, fibrosis, central, caspase, hepatology, mice, fibrogenesis, access, cell, hepatocyte, caspases, injury, expression, activation, privacy, cookies, content, mcd, diet, steatosis, gores, information, publish, research, search, death, model, thapaliya, wree, berk, dixon, casp, inflammation, showed, ccr, open, dis, gastroenterology,

Topics {✒️}

month download article/chapter high fat diet-induced diet-induced nash model wt mcd-fed mice pan-caspase inhibitor emricasan article digestive diseases inflammatory gr1 + monocyte subset population-based cohort study mcd diet showed hepatic stellate cells stimulating tnf-alpha expression maria eugenia inzaugarat & ariel full article pdf related subjects nash-related apoptosis decreases liver injury privacy choices/manage cookies lerner research institute hepatic cell death innate immune cells maria eugenia inzaugarat liver cell apoptosis control cell death semin liver dis elevated liver enzymes central regulator article thapaliya fatty liver clin liver dis mcd showed human nonalcoholic steatohepatitis 2016 cxcl10-mediates macrophage intrahepatic monocyte subsets pan-caspase inhibition liver injury liver disease european economic area curr opin pediatr invasive versus noninvasive long-term follow histological scoring system shape caspase activity check access instant access annu rev biochem hepatic steatosis sensitizes conditions privacy policy ccr2-dependent infiltration feldstein ae article log

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Caspase 3 Inactivation Protects Against Hepatic Cell Death and Ameliorates Fibrogenesis in a Diet-Induced NASH Model
         description:Hepatocyte cell death is a key feature of nonalcoholic steatohepatitis (NASH). As the contribution of specific caspases remains unclear, our aim was to ascertain the effect of caspase 3 suppression on liver injury and fibrogenesis. C57BL/6 wild-type (WT) and caspase 3 knock out (Casp3 −/−) mice were placed on a methionine- and choline-deficient (MCD) diet for 6 weeks to induce steatohepatitis and liver fibrosis. Thereafter, liver injury, liver fibrosis and hepatocellular apoptosis were quantified in liver sections. Additionally, expression of proteins associated with liver inflammation and fibrogenesis was analyzed. WT mice fed MCD diet showed marked activation of caspase 3 in hepatocytes, in conjunction with steatohepatitis and increased hepatic triglyceride levels, hepatocyte ballooning, inflammation and fibrosis. Casp3 −/− mice fed the MCD diet showed similar serum aminotransferase levels and NAFLD activity scores (NAS) compared with WT MCD-fed mice. However, Casp3 −/− mice on the MCD diet showed a marked reduction in expression of transcripts for profibrogenic genes, which translated into reduced hepatic collagen deposition. These changes were associated with decreased levels of apoptosis, and a significant reduction in the expression of cytokines involved in inflammatory signaling. Casp3 −/− mice on the MCD showed a reduction in expression of chemokine receptor 2 (CCR2) leading to ameliorated infiltration of inflammatory lymphocyte antigen 6 complex, locus C1 (Ly6c) positive monocytes. These findings support a prominent role for hepatocyte caspase 3 activation in NASH-related apoptosis, fibrogenesis and fibrosis which in part is mediated via CCR2-dependent infiltration of Ly6c positive monocytes.
         datePublished:2014-05-03T00:00:00Z
         dateModified:2014-05-03T00:00:00Z
         pageStart:1197
         pageEnd:1206
         sameAs:https://doi.org/10.1007/s10620-014-3167-6
         keywords:
            Nonalcoholic fatty liver disease
            Caspases
            Apoptosis
            Liver injury
            Liver fibrosis
            Gastroenterology
            Hepatology
            Oncology
            Transplant Surgery
            Biochemistry
            general
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig2_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig3_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig4_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig5_HTML.gif
         isPartOf:
            name:Digestive Diseases and Sciences
            issn:
               1573-2568
               0163-2116
            volumeNumber:59
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer US
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Samjhana Thapaliya
               affiliation:
                     name:Cleveland Clinic
                     address:
                        name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Alexander Wree
               affiliation:
                     name:University of California, San Diego
                     address:
                        name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Davide Povero
               affiliation:
                     name:University of California, San Diego
                     address:
                        name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Maria Eugenia Inzaugarat
               affiliation:
                     name:University of California, San Diego
                     address:
                        name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Michael Berk
               affiliation:
                     name:Cleveland Clinic
                     address:
                        name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Laura Dixon
               affiliation:
                     name:Cleveland Clinic
                     address:
                        name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Bettina G. Papouchado
               affiliation:
                     name:University of California, San Diego
                     address:
                        name:Department of Pathology, University of California, San Diego, La Jolla, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Ariel E. Feldstein
               affiliation:
                     name:University of California, San Diego
                     address:
                        name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Caspase 3 Inactivation Protects Against Hepatic Cell Death and Ameliorates Fibrogenesis in a Diet-Induced NASH Model
      description:Hepatocyte cell death is a key feature of nonalcoholic steatohepatitis (NASH). As the contribution of specific caspases remains unclear, our aim was to ascertain the effect of caspase 3 suppression on liver injury and fibrogenesis. C57BL/6 wild-type (WT) and caspase 3 knock out (Casp3 −/−) mice were placed on a methionine- and choline-deficient (MCD) diet for 6 weeks to induce steatohepatitis and liver fibrosis. Thereafter, liver injury, liver fibrosis and hepatocellular apoptosis were quantified in liver sections. Additionally, expression of proteins associated with liver inflammation and fibrogenesis was analyzed. WT mice fed MCD diet showed marked activation of caspase 3 in hepatocytes, in conjunction with steatohepatitis and increased hepatic triglyceride levels, hepatocyte ballooning, inflammation and fibrosis. Casp3 −/− mice fed the MCD diet showed similar serum aminotransferase levels and NAFLD activity scores (NAS) compared with WT MCD-fed mice. However, Casp3 −/− mice on the MCD diet showed a marked reduction in expression of transcripts for profibrogenic genes, which translated into reduced hepatic collagen deposition. These changes were associated with decreased levels of apoptosis, and a significant reduction in the expression of cytokines involved in inflammatory signaling. Casp3 −/− mice on the MCD showed a reduction in expression of chemokine receptor 2 (CCR2) leading to ameliorated infiltration of inflammatory lymphocyte antigen 6 complex, locus C1 (Ly6c) positive monocytes. These findings support a prominent role for hepatocyte caspase 3 activation in NASH-related apoptosis, fibrogenesis and fibrosis which in part is mediated via CCR2-dependent infiltration of Ly6c positive monocytes.
      datePublished:2014-05-03T00:00:00Z
      dateModified:2014-05-03T00:00:00Z
      pageStart:1197
      pageEnd:1206
      sameAs:https://doi.org/10.1007/s10620-014-3167-6
      keywords:
         Nonalcoholic fatty liver disease
         Caspases
         Apoptosis
         Liver injury
         Liver fibrosis
         Gastroenterology
         Hepatology
         Oncology
         Transplant Surgery
         Biochemistry
         general
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig3_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig4_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10620-014-3167-6/MediaObjects/10620_2014_3167_Fig5_HTML.gif
      isPartOf:
         name:Digestive Diseases and Sciences
         issn:
            1573-2568
            0163-2116
         volumeNumber:59
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Samjhana Thapaliya
            affiliation:
                  name:Cleveland Clinic
                  address:
                     name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Alexander Wree
            affiliation:
                  name:University of California, San Diego
                  address:
                     name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Davide Povero
            affiliation:
                  name:University of California, San Diego
                  address:
                     name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Maria Eugenia Inzaugarat
            affiliation:
                  name:University of California, San Diego
                  address:
                     name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Michael Berk
            affiliation:
                  name:Cleveland Clinic
                  address:
                     name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Laura Dixon
            affiliation:
                  name:Cleveland Clinic
                  address:
                     name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Bettina G. Papouchado
            affiliation:
                  name:University of California, San Diego
                  address:
                     name:Department of Pathology, University of California, San Diego, La Jolla, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ariel E. Feldstein
            affiliation:
                  name:University of California, San Diego
                  address:
                     name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Digestive Diseases and Sciences
      issn:
         1573-2568
         0163-2116
      volumeNumber:59
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Cleveland Clinic
      address:
         name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
         type:PostalAddress
      name:University of California, San Diego
      address:
         name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
         type:PostalAddress
      name:University of California, San Diego
      address:
         name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
         type:PostalAddress
      name:University of California, San Diego
      address:
         name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
         type:PostalAddress
      name:Cleveland Clinic
      address:
         name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
         type:PostalAddress
      name:Cleveland Clinic
      address:
         name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
         type:PostalAddress
      name:University of California, San Diego
      address:
         name:Department of Pathology, University of California, San Diego, La Jolla, USA
         type:PostalAddress
      name:University of California, San Diego
      address:
         name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Samjhana Thapaliya
      affiliation:
            name:Cleveland Clinic
            address:
               name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
               type:PostalAddress
            type:Organization
      name:Alexander Wree
      affiliation:
            name:University of California, San Diego
            address:
               name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
               type:PostalAddress
            type:Organization
      name:Davide Povero
      affiliation:
            name:University of California, San Diego
            address:
               name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
               type:PostalAddress
            type:Organization
      name:Maria Eugenia Inzaugarat
      affiliation:
            name:University of California, San Diego
            address:
               name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
               type:PostalAddress
            type:Organization
      name:Michael Berk
      affiliation:
            name:Cleveland Clinic
            address:
               name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
               type:PostalAddress
            type:Organization
      name:Laura Dixon
      affiliation:
            name:Cleveland Clinic
            address:
               name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
               type:PostalAddress
            type:Organization
      name:Bettina G. Papouchado
      affiliation:
            name:University of California, San Diego
            address:
               name:Department of Pathology, University of California, San Diego, La Jolla, USA
               type:PostalAddress
            type:Organization
      name:Ariel E. Feldstein
      affiliation:
            name:University of California, San Diego
            address:
               name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
      name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
      name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
      name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
      name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
      name:Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, USA
      name:Department of Pathology, University of California, San Diego, La Jolla, USA
      name:Department of Pediatrics, University of California, San Diego, La Jolla, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(166)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

3.73s.

LINK . SPRINGER . COM {}