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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
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We are analyzing https://link.springer.com/article/10.1007/s00467-018-3984-5.

Title:
Mitochondrial mechanisms and therapeutics in ischaemia reperfusion injury | Pediatric Nephrology
Description:
Acute kidney injury (AKI) remains a major problem in critically unwell children and young adults. Ischaemia reperfusion (IR) injury is a major contributor to the development of AKI in a significant proportion of these cases and mitochondria are increasingly recognised as being central to this process through generation of a burst of reactive oxygen species early in reperfusion. Mitochondria have additionally been shown to have key roles in downstream processes including activation of the immune response, immunomodulation, and apoptosis and necrosis. The recognition of the central role of mitochondria in IR injury and an increased understanding of the pathophysiology that undermines these processes has resulted in identification of novel therapeutic targets and potential biomarkers. This review summarises a variety of therapeutic approaches that are currently under exploration and may have potential in ameliorating AKI in children in the future.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Health & Fitness
  • Fitness & Wellness
  • Insurance

Content Management System {πŸ“}

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 {πŸ“ˆ}

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? {πŸ’Έ}

We can't tell how the site generates income.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {πŸ”}

pubmed, mitochondrial, injury, article, google, scholar, cas, kidney, mitochondria, central, aki, acute, shown, renal, reperfusion, succinate, ischaemia, murphy, oxygen, ros, dna, role, patients, cell, immune, reactive, species, response, therapeutic, mtdna, function, generation, activation, vivo, models, nephrol, including, potential, ischemiareperfusion, children, apoptosis, tissue, damage, mitoq, research, saebparsy, recognised, necrosis, pathway, cellular,

Topics {βœ’οΈ}

titze-de-almeida ss full size image dynamic contrast-enhanced mri article download pdf insulin-dependent diabetes mellitus m2 anti-inflammatory cells long-term graft survival ischaemic damage-induced loss transcription factor nf-ΞΊb chain-breaking antioxidant ubiquinol mito-qc illuminates mitophagy medical research council mitochondria-targeted antioxidant mitoq reactive oxygen species human ischemia-reperfusion injury limit pro-inflammatory responses kidney ischemia/reperfusion injury pgc-1alpha promotes recovery renal ischemia-reperfusion injury longer-term renal function kourosh saeb-parsy pro-apoptotic protein bak acute kidney injury sirt1/pgc-1alpha activation anti-inflammatory metabolite er-linked sting pathway apoptosis-based therapeutic agents acute renal injury mitochondrial-targeted compound ss-31 energizes ischemic mitochondria lung injury induced proximal tubular injury transplant research unit autophagy-related protein 7 full access chain breaking antioxidant privacy choices/manage cookies cell death induced acute tubular necrosis inter-species difference tubular epithelial cells small interfering rna outer mitochondrial membrane myocardial necrosis induced targeted click chemistry chronic kidney disease underlie tubular injury pro-inflammatory agent proximal tubules protects short-term outcomes

Questions {❓}

  • Braunwald E, Kloner RA (1985) Myocardial reperfusion: a double-edged sword?
  • Hearse DJ, Humphrey SM, Bullock GR (1978) The oxygen paradox and the calcium paradox: two facets of the same problem?
  • Ullmann LP (1981) Cognitions: help or hindrance?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Mitochondrial mechanisms and therapeutics in ischaemia reperfusion injury
         description:Acute kidney injury (AKI) remains a major problem in critically unwell children and young adults. Ischaemia reperfusion (IR) injury is a major contributor to the development of AKI in a significant proportion of these cases and mitochondria are increasingly recognised as being central to this process through generation of a burst of reactive oxygen species early in reperfusion. Mitochondria have additionally been shown to have key roles in downstream processes including activation of the immune response, immunomodulation, and apoptosis and necrosis. The recognition of the central role of mitochondria in IR injury and an increased understanding of the pathophysiology that undermines these processes has resulted in identification of novel therapeutic targets and potential biomarkers. This review summarises a variety of therapeutic approaches that are currently under exploration and may have potential in ameliorating AKI in children in the future.
         datePublished:2018-06-02T00:00:00Z
         dateModified:2018-06-02T00:00:00Z
         pageStart:1167
         pageEnd:1174
         sameAs:https://doi.org/10.1007/s00467-018-3984-5
         keywords:
            Acute kidney injury
            Children
            Ischaemia reperfusion injury
            Mitochondria
            Reactive oxygen species
            Succinate
            Pediatrics
            Nephrology
            Urology
         image:
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         isPartOf:
            name:Pediatric Nephrology
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               name:Jack L. Martin
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                     address:
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ScholarlyArticle:
      headline:Mitochondrial mechanisms and therapeutics in ischaemia reperfusion injury
      description:Acute kidney injury (AKI) remains a major problem in critically unwell children and young adults. Ischaemia reperfusion (IR) injury is a major contributor to the development of AKI in a significant proportion of these cases and mitochondria are increasingly recognised as being central to this process through generation of a burst of reactive oxygen species early in reperfusion. Mitochondria have additionally been shown to have key roles in downstream processes including activation of the immune response, immunomodulation, and apoptosis and necrosis. The recognition of the central role of mitochondria in IR injury and an increased understanding of the pathophysiology that undermines these processes has resulted in identification of novel therapeutic targets and potential biomarkers. This review summarises a variety of therapeutic approaches that are currently under exploration and may have potential in ameliorating AKI in children in the future.
      datePublished:2018-06-02T00:00:00Z
      dateModified:2018-06-02T00:00:00Z
      pageStart:1167
      pageEnd:1174
      sameAs:https://doi.org/10.1007/s00467-018-3984-5
      keywords:
         Acute kidney injury
         Children
         Ischaemia reperfusion injury
         Mitochondria
         Reactive oxygen species
         Succinate
         Pediatrics
         Nephrology
         Urology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00467-018-3984-5/MediaObjects/467_2018_3984_Fig1_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00467-018-3984-5/MediaObjects/467_2018_3984_Fig2_HTML.png
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      isPartOf:
         name:Pediatric Nephrology
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            1432-198X
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         volumeNumber:34
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         name:Springer Berlin Heidelberg
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            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
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      author:
            name:Jack L. Martin
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            name:Anja V. Gruszczyk
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                     name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK
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            name:Kourosh Saeb-Parsy
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                     name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK
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               name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK
               type:PostalAddress
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            name:University of Cambridge
            address:
               name:MRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Anja V. Gruszczyk
      affiliation:
            name:University of Cambridge
            address:
               name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
            name:University of Cambridge
            address:
               name:MRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Timothy E. Beach
      affiliation:
            name:University of Cambridge
            address:
               name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Michael P. Murphy
      affiliation:
            name:University of Cambridge
            address:
               name:MRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Kourosh Saeb-Parsy
      affiliation:
            name:University of Cambridge
            address:
               name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK
      name:MRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, UK
      name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK
      name:MRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, UK
      name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK
      name:MRC Mitochondrial Biology Unit, Biomedical Campus, University of Cambridge, Cambridge, UK
      name:Department of Surgery and Cambridge NIHR Biomedical Research Centre, Biomedical Campus, University of Cambridge, Cambridge, UK

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