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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Schema
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. Hosting Providers
  13. CDN Services

We began analyzing https://link.springer.com/article/10.1007/s10863-009-9205-y, but it redirected us to https://link.springer.com/article/10.1007/s10863-009-9205-y. The analysis below is for the second page.

Title[redir]:
Akt mediated mitochondrial protection in the heart: metabolic and survival pathways to the rescue | Journal of Bioenergetics and Biomembranes
Description:
Cardiomyocyte death is now recognized as a critical factor in the development of heart disease. Mitochondria are not only responsible for energy production to ensure that cardiac output meets the body’s energy demands, but they serve as critical integrators of cell survival signals. Numerous stressors are known to induce cell death by necrosis and/or apoptosis mediated through mitochondrial dysregulation. Anti- and pro-apoptotic Bcl-2 family proteins regulate apoptosis by controlling mitochondrial outer membrane permeability, whereas opening of the mitochondrial permeability transition pore (PT-pore) induces large amplitude permeability of the inner membrane and consequent rupture of the outer membrane. Akt is one of the best described survival kinases activated by receptor ligands and its activation preserves mitochondrial integrity and protects cardiomyocytes against necrotic and apoptotic death. The mechanisms responsible for Akt-mediated mitochondrial protection have not been fully elucidated. There is, however, accumulating evidence that multiple Akt target molecules, recruited through both transcriptional and post-transcriptional mechanisms, directly impinge upon and protect mitochondria. In this review we discuss mechanisms by which Akt activation can effect changes at the mitochondria that protect cardiomyocytes and attenuate pathophysiological responses of the heart.

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

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


Based on our best estimate, this website will receive around 9,135,289 visitors per month in the current month.

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How Does Doi.org 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. Doi.org could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

google, scholar, cas, biol, cell, chem, physiol, circ, mol, heart, res, brown, cardiol, article, death, circulation, mitochondrial, murphy, wang, chen, miyamoto, zhang, clin, akt, access, mitochondria, biochem, dorn, med, robey, science, invest, privacy, cookies, journal, open, curr, gottlieb, molkentin, nature, yellon, hay, differ, proc, natl, acad, sci, content, protection, publish,

Topics {✒️}

akt-mediated mitochondrial protection murphy & joan heller brown atp-sensitive potassium channel adams jw de gomez-puyou mt article download pdf privacy choices/manage cookies apoptosis mediated main content log dorn gw 2nd european economic area cardiac output meets attenuate pathophysiological responses related subjects florez-mcclure ml van der kaay conditions privacy policy de felice fg induce cell death survival kinases activated journal finder publish cell survival signals accepting optional cookies pimentel-muinos fx lammers jw gustafsson ab baines cp full access apoptotic death mitochondrial dysregulation post-transcriptional mechanisms crow mt article miyamoto heart disease means ck zorov db printz rl reed jc rathmell jc akt activation data protection green dr plas dr halestrap ap search search dorn gw brown mt downey jm gomez-puyou shigeki miyamoto

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Akt mediated mitochondrial protection in the heart: metabolic and survival pathways to the rescue
         description:Cardiomyocyte death is now recognized as a critical factor in the development of heart disease. Mitochondria are not only responsible for energy production to ensure that cardiac output meets the body’s energy demands, but they serve as critical integrators of cell survival signals. Numerous stressors are known to induce cell death by necrosis and/or apoptosis mediated through mitochondrial dysregulation. Anti- and pro-apoptotic Bcl-2 family proteins regulate apoptosis by controlling mitochondrial outer membrane permeability, whereas opening of the mitochondrial permeability transition pore (PT-pore) induces large amplitude permeability of the inner membrane and consequent rupture of the outer membrane. Akt is one of the best described survival kinases activated by receptor ligands and its activation preserves mitochondrial integrity and protects cardiomyocytes against necrotic and apoptotic death. The mechanisms responsible for Akt-mediated mitochondrial protection have not been fully elucidated. There is, however, accumulating evidence that multiple Akt target molecules, recruited through both transcriptional and post-transcriptional mechanisms, directly impinge upon and protect mitochondria. In this review we discuss mechanisms by which Akt activation can effect changes at the mitochondria that protect cardiomyocytes and attenuate pathophysiological responses of the heart.
         datePublished:2009-04-18T00:00:00Z
         dateModified:2009-04-18T00:00:00Z
         pageStart:169
         pageEnd:180
         license:https://creativecommons.org/licenses/by-nc/2.0
         sameAs:https://doi.org/10.1007/s10863-009-9205-y
         keywords:
            Akt
            Mitochondria
            Heart
            Hexokinase-II
            Bioorganic Chemistry
            Biochemistry
            general
            Animal Anatomy / Morphology / Histology
            Animal Biochemistry
            Organic Chemistry
         image:
         isPartOf:
            name:Journal of Bioenergetics and Biomembranes
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            volumeNumber:41
            type:
               Periodical
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            name:Springer US
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               type:ImageObject
            type:Organization
         author:
               name:Shigeki Miyamoto
               affiliation:
                     name:University of California
                     address:
                        name:Department of Pharmacology, University of California, San Diego, USA
                        type:PostalAddress
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               type:Person
               name:Anne N. Murphy
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                     name:University of California
                     address:
                        name:Department of Pharmacology, University of California, San Diego, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Joan Heller Brown
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                     name:University of California
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                        name:Department of Pharmacology, University of California, San Diego, USA
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      context:https://schema.org
ScholarlyArticle:
      headline:Akt mediated mitochondrial protection in the heart: metabolic and survival pathways to the rescue
      description:Cardiomyocyte death is now recognized as a critical factor in the development of heart disease. Mitochondria are not only responsible for energy production to ensure that cardiac output meets the body’s energy demands, but they serve as critical integrators of cell survival signals. Numerous stressors are known to induce cell death by necrosis and/or apoptosis mediated through mitochondrial dysregulation. Anti- and pro-apoptotic Bcl-2 family proteins regulate apoptosis by controlling mitochondrial outer membrane permeability, whereas opening of the mitochondrial permeability transition pore (PT-pore) induces large amplitude permeability of the inner membrane and consequent rupture of the outer membrane. Akt is one of the best described survival kinases activated by receptor ligands and its activation preserves mitochondrial integrity and protects cardiomyocytes against necrotic and apoptotic death. The mechanisms responsible for Akt-mediated mitochondrial protection have not been fully elucidated. There is, however, accumulating evidence that multiple Akt target molecules, recruited through both transcriptional and post-transcriptional mechanisms, directly impinge upon and protect mitochondria. In this review we discuss mechanisms by which Akt activation can effect changes at the mitochondria that protect cardiomyocytes and attenuate pathophysiological responses of the heart.
      datePublished:2009-04-18T00:00:00Z
      dateModified:2009-04-18T00:00:00Z
      pageStart:169
      pageEnd:180
      license:https://creativecommons.org/licenses/by-nc/2.0
      sameAs:https://doi.org/10.1007/s10863-009-9205-y
      keywords:
         Akt
         Mitochondria
         Heart
         Hexokinase-II
         Bioorganic Chemistry
         Biochemistry
         general
         Animal Anatomy / Morphology / Histology
         Animal Biochemistry
         Organic Chemistry
      image:
      isPartOf:
         name:Journal of Bioenergetics and Biomembranes
         issn:
            1573-6881
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            Periodical
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         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Shigeki Miyamoto
            affiliation:
                  name:University of California
                  address:
                     name:Department of Pharmacology, University of California, San Diego, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Anne N. Murphy
            affiliation:
                  name:University of California
                  address:
                     name:Department of Pharmacology, University of California, San Diego, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Joan Heller Brown
            affiliation:
                  name:University of California
                  address:
                     name:Department of Pharmacology, University of California, San Diego, USA
                     type:PostalAddress
                  type:Organization
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      name:Journal of Bioenergetics and Biomembranes
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      name:Springer US
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      name:University of California
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         name:Department of Pharmacology, University of California, San Diego, USA
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      name:University of California
      address:
         name:Department of Pharmacology, University of California, San Diego, USA
         type:PostalAddress
      name:University of California
      address:
         name:Department of Pharmacology, University of California, San Diego, USA
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      name:Shigeki Miyamoto
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            name:University of California
            address:
               name:Department of Pharmacology, University of California, San Diego, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Anne N. Murphy
      affiliation:
            name:University of California
            address:
               name:Department of Pharmacology, University of California, San Diego, USA
               type:PostalAddress
            type:Organization
      name:Joan Heller Brown
      affiliation:
            name:University of California
            address:
               name:Department of Pharmacology, University of California, San Diego, USA
               type:PostalAddress
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      name:Department of Pharmacology, University of California, San Diego, USA
      name:Department of Pharmacology, University of California, San Diego, USA
      name:Department of Pharmacology, University of California, San Diego, USA

External Links {🔗}(371)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {📦}

  • Crossref

5.84s.