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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. Schema
  9. External Links
  10. Analytics And Tracking
  11. Libraries

We are analyzing https://link.springer.com/article/10.1007/s00395-006-0622-3.

Title:
Impairment of cardioprotective PI3K-Akt signaling by post-infarct ventricular remodeling is compensated by an ERK-mediated pathway | Basic Research in Cardiology
Description:
Recently we found that post-infarct remodeling disrupts PI3KAkt signaling triggered by erythropoietin (EPO) but an unknown compensatory mechanism preserves EPO-induced protection against infarction in those hearts. In this study, we examined the possibility that ERK-mediated signaling is the compensatory mechanism affording protection in post-infarct remodeled hearts. Four weeks after coronary ligation in situ (post-MI group, post-MI) or a sham operation (sham group, Sham), hearts were isolated, perfused and subjected to 25-min global ischemia/2-h reperfusion. Infarct size was expressed as a percentage of risk area size (%I/R), from which scarred infarct by coronary ligation was excluded. EPO infusion (5 U/ml) before ischemia reduced %I/R similarly in Sham and post-MI (from 62.0 ± 5.1 to 39.4 ± 4.8 in Sham and from 58.6 ± 6.6 to 36.3 ± 3.8 in post-MI). PD98059, a MEK1/2 inhibitor, abolished this EPO-induced protection in post-MI (%I/R = 60.7 ± 4.9) but not in Sham (%I/R = 35.1 ± 5.4). EPO induced PI3Kdependent phosphorylation of Akt in Sham but not in post-MI. EPO increased phosphorylation levels of ERK1/2 both in Sham and post-MI, but this phosphorylation was diminished by a PI3K inhibitor in Sham but not in post-MI. These results suggest that PI3K-independent activation of ERK compensates the lack of signal input from the PI3K-Akt pathway to achieve EPO-induced protection in the remodeled myocardium.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Insurance
  • Non-Profit & Charity

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're unsure if the website is profiting.

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 have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

article, google, scholar, cas, pubmed, signaling, miura, sham, miki, erythropoietin, postmi, activation, myocardial, kinase, basic, postinfarct, remodeling, pathway, tanno, shimamoto, protection, ventricular, hearts, erk, access, privacy, cookies, content, research, pikakt, infarction, phosphorylation, signal, res, preconditioning, publish, search, cardioprotective, nishihara, takahashi, epo, mechanism, remodeled, coronary, infarct, size, effect, ischemic, injury, cardiol,

Topics {✒️}

month download article/chapter glycogen synthase kinase-3β cardioprotective pi3k-akt signaling post-infarct remodeled hearts post-infarct ventricular remodeling erythropoietin-induced cardioprotective signaling achieve epo-induced protection erythropoietin-mediated acute protection article basic research myocardial infarct size pi3k-akt pathway erk-mediated signaling p44/p42 mapks phosphatidylinositol- 3-kinase signaling phosphatidylinositol 3-kinase signaling epo-induced protection postinfarct remodeled hearts postinfarct ventricular remodeling full article pdf myocardial ischemia/reperfusion injury privacy choices/manage cookies erk-mediated pathway risk area size pi3k-independent activation erythropoietin-mediated cardioprotection acute myocardial infarction primary erythroid progenitors infarct size factorial randomized trial primes gsk-3β signal transduction mediated remote ischemic conditioning pkc-dependent activation prior myocardial infarction ventricular remodeling european economic area scope submit manuscript prodromal angina pectoris pkc-ε underlies van de werf protein kinase ischaemic preconditioning effect conditions privacy policy myocardial ischemia-reperfusion turning cells red https 25-min global ischemia/2 article miki impaired myocardial response ischemia- reperfusion injury

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Impairment of cardioprotective PI3K-Akt signaling by post-infarct ventricular remodeling is compensated by an ERK-mediated pathway
         description:Recently we found that post-infarct remodeling disrupts PI3KAkt signaling triggered by erythropoietin (EPO) but an unknown compensatory mechanism preserves EPO-induced protection against infarction in those hearts. In this study, we examined the possibility that ERK-mediated signaling is the compensatory mechanism affording protection in post-infarct remodeled hearts. Four weeks after coronary ligation in situ (post-MI group, post-MI) or a sham operation (sham group, Sham), hearts were isolated, perfused and subjected to 25-min global ischemia/2-h reperfusion. Infarct size was expressed as a percentage of risk area size (%I/R), from which scarred infarct by coronary ligation was excluded. EPO infusion (5 U/ml) before ischemia reduced %I/R similarly in Sham and post-MI (from 62.0 ± 5.1 to 39.4 ± 4.8 in Sham and from 58.6 ± 6.6 to 36.3 ± 3.8 in post-MI). PD98059, a MEK1/2 inhibitor, abolished this EPO-induced protection in post-MI (%I/R = 60.7 ± 4.9) but not in Sham (%I/R = 35.1 ± 5.4). EPO induced PI3Kdependent phosphorylation of Akt in Sham but not in post-MI. EPO increased phosphorylation levels of ERK1/2 both in Sham and post-MI, but this phosphorylation was diminished by a PI3K inhibitor in Sham but not in post-MI. These results suggest that PI3K-independent activation of ERK compensates the lack of signal input from the PI3K-Akt pathway to achieve EPO-induced protection in the remodeled myocardium.
         datePublished:2006-09-01T00:00:00Z
         dateModified:2006-09-01T00:00:00Z
         pageStart:163
         pageEnd:170
         sameAs:https://doi.org/10.1007/s00395-006-0622-3
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            erythropoietin
            PI3K-Akt
            ERK
            remodeled hearts
            infarct size
            Cardiology
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ScholarlyArticle:
      headline:Impairment of cardioprotective PI3K-Akt signaling by post-infarct ventricular remodeling is compensated by an ERK-mediated pathway
      description:Recently we found that post-infarct remodeling disrupts PI3KAkt signaling triggered by erythropoietin (EPO) but an unknown compensatory mechanism preserves EPO-induced protection against infarction in those hearts. In this study, we examined the possibility that ERK-mediated signaling is the compensatory mechanism affording protection in post-infarct remodeled hearts. Four weeks after coronary ligation in situ (post-MI group, post-MI) or a sham operation (sham group, Sham), hearts were isolated, perfused and subjected to 25-min global ischemia/2-h reperfusion. Infarct size was expressed as a percentage of risk area size (%I/R), from which scarred infarct by coronary ligation was excluded. EPO infusion (5 U/ml) before ischemia reduced %I/R similarly in Sham and post-MI (from 62.0 ± 5.1 to 39.4 ± 4.8 in Sham and from 58.6 ± 6.6 to 36.3 ± 3.8 in post-MI). PD98059, a MEK1/2 inhibitor, abolished this EPO-induced protection in post-MI (%I/R = 60.7 ± 4.9) but not in Sham (%I/R = 35.1 ± 5.4). EPO induced PI3Kdependent phosphorylation of Akt in Sham but not in post-MI. EPO increased phosphorylation levels of ERK1/2 both in Sham and post-MI, but this phosphorylation was diminished by a PI3K inhibitor in Sham but not in post-MI. These results suggest that PI3K-independent activation of ERK compensates the lack of signal input from the PI3K-Akt pathway to achieve EPO-induced protection in the remodeled myocardium.
      datePublished:2006-09-01T00:00:00Z
      dateModified:2006-09-01T00:00:00Z
      pageStart:163
      pageEnd:170
      sameAs:https://doi.org/10.1007/s00395-006-0622-3
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         erythropoietin
         PI3K-Akt
         ERK
         remodeled hearts
         infarct size
         Cardiology
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            name:T. Miki
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                  name:Sapporo Medical University School of Medicine
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                     name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
                     type:PostalAddress
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            name:T. Miura
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                  name:Sapporo Medical University School of Medicine
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      affiliation:
            name:Sapporo Medical University School of Medicine
            address:
               name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
               type:PostalAddress
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            address:
               name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
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            name:Sapporo Medical University School of Medicine
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            name:Sapporo Medical University School of Medicine
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      name:M. Nishihara
      affiliation:
            name:Sapporo Medical University School of Medicine
            address:
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            address:
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      name:T. Sato
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            name:Sapporo Medical University School of Medicine
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               name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
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      affiliation:
            name:Sapporo Medical University School of Medicine
            address:
               name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
               type:PostalAddress
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      name:K. Shimamoto
      affiliation:
            name:Sapporo Medical University School of Medicine
            address:
               name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
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      name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
      name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
      name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
      name:Dept. of Pharmacology, Sapporo Medical University School of Medicine, Sapporo, Japan
      name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
      name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
      name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
      name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
      name:Second Dept. of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
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External Links {🔗}(98)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
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