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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. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers
  14. CDN Services

We began analyzing https://link.springer.com/article/10.1007/s00395-015-0520-7, but it redirected us to https://link.springer.com/article/10.1007/s00395-015-0520-7. The analysis below is for the second page.

Title[redir]:
Emerging role of liver X receptors in cardiac pathophysiology and heart failure | Basic Research in Cardiology
Description:
Liver X receptors (LXRs) are master regulators of metabolism and have been studied for their pharmacological potential in vascular and metabolic disease. Besides their established role in metabolic homeostasis and disease, there is mounting evidence to suggest that LXRs may exert direct beneficial effects in the heart. Here, we aim to provide a conceptual framework to explain the broad mode of action of LXRs and how LXR signaling may be an important local and systemic target for the treatment of heart failure. We discuss the potential role of LXRs in systemic conditions associated with heart failure, such as hypertension, diabetes, and renal and vascular disease. Further, we expound on recent data that implicate a direct role for LXR activation in the heart, for its impact on cardiomyocyte damage and loss due to ischemia, and effects on cardiac hypertrophy, fibrosis, and myocardial metabolism. Taken together, the accumulating evidence supports the notion that LXRs may represent a novel therapeutic target for the treatment of heart failure.

Matching Content Categories {📚}

  • Health & Fitness
  • Science
  • Education

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?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 98,426,998 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.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Doi.org might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

pubmed, article, google, scholar, cas, heart, lxr, liver, lxrs, receptor, failure, activation, cardiac, central, myocardial, lxrα, glucose, diabetes, mice, disease, effects, signaling, receptors, role, remodeling, cell, metabolic, cholesterol, expression, gene, insulin, pii, metabolism, agonist, van, vascular, lipid, dysfunction, increased, atherosclerosis, hypertrophy, target, cells, chronic, growth, function, injury, endothelial, biol, wang,

Topics {✒️}

lxrα/β-deficient ob/ob mice prevented hypoxia-reoxygenation-induced apoptosis bsp/cpd/e-pub/000724 [pii] cardiac renin-angiotensin-aldosterone system carbohydrate-response element-binding protein suppressing nf-kappab signalling thyroid hormone-responsive elements article download pdf renin-angiotensin-aldosterone system n-dimethyl-3β-hydroxycholenamide liver-x-receptor beta protects entero-hepatic sterol absorption renin-angiotensin system antagonists amp-activated protein kinase insulin-stimulated as160 phosphorylation high-fat fed rats counteract pro-fibrotic signaling receptor-alpha reduces activation potent anti-hypertrophic effectors multi-organ dysfunction involving extracellular matrix turnover keap-1/nrf-2 signaling pathways streptozotocin-induced diabetic rats β-cell insulin secretion lxrα-encoding gene nr1h3 downstream posttranslational o-glcnacylation infarct-sparing effects occurred db/db diabetic mouse oxidized low-density lipoprotein pro-fibrotic gene expression hyperglycemia-induced renal damage tac-induced pressure overload macrophage-derived lxr signaling at1 receptor-dependent activation glucose-activated transcription factor exerts anti-fibrotic effects hyperglycemic-induced kidney disease camp-responsive transcriptional regulator mitochondria-mediated apoptotic pathways aibp-mediated cholesterol efflux ligand-activated transcription factors liver x-receptor agonist liver-x-receptor alpha lxr-dependent gene expression lxr-null mice lost anti-apoptotic factor aim liver-x-receptor ligand post-ischemic myocardial apoptosis adrenergic-fatty acid load lxr/rxr complex undergoes

Questions {❓}

  • Rankinen T, Sarzynski MA, Ghosh S, Bouchard C (2015) Are there genetic paths common to obesity, cardiovascular disease outcomes, and cardiovascular risk factors?
  • Viennois E, Pommier AJ, Mouzat K, Oumeddour A, El Hajjaji FZ, Dufour J, Caira F, Volle DH, Baron S, Lobaccaro JM (2011) Targeting liver X receptors in human health: deadlock or promising trail?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Emerging role of liver X receptors in cardiac pathophysiology and heart failure
         description:Liver X receptors (LXRs) are master regulators of metabolism and have been studied for their pharmacological potential in vascular and metabolic disease. Besides their established role in metabolic homeostasis and disease, there is mounting evidence to suggest that LXRs may exert direct beneficial effects in the heart. Here, we aim to provide a conceptual framework to explain the broad mode of action of LXRs and how LXR signaling may be an important local and systemic target for the treatment of heart failure. We discuss the potential role of LXRs in systemic conditions associated with heart failure, such as hypertension, diabetes, and renal and vascular disease. Further, we expound on recent data that implicate a direct role for LXR activation in the heart, for its impact on cardiomyocyte damage and loss due to ischemia, and effects on cardiac hypertrophy, fibrosis, and myocardial metabolism. Taken together, the accumulating evidence supports the notion that LXRs may represent a novel therapeutic target for the treatment of heart failure.
         datePublished:2015-11-26T00:00:00Z
         dateModified:2015-11-26T00:00:00Z
         pageStart:1
         pageEnd:17
         license:http://creativecommons.org/licenses/by/4.0/
         sameAs:https://doi.org/10.1007/s00395-015-0520-7
         keywords:
            Cardiac remodeling
            Cardiovascular risk factors
            Heart failure
            Hypertrophy
            Liver X receptors
            Metabolism
            Cardiology
         image:
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         isPartOf:
            name:Basic Research in Cardiology
            issn:
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            volumeNumber:111
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               name:Megan V. Cannon
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                     name:University of Groningen, University Medical Center Groningen
                     address:
                        name:Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
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ScholarlyArticle:
      headline:Emerging role of liver X receptors in cardiac pathophysiology and heart failure
      description:Liver X receptors (LXRs) are master regulators of metabolism and have been studied for their pharmacological potential in vascular and metabolic disease. Besides their established role in metabolic homeostasis and disease, there is mounting evidence to suggest that LXRs may exert direct beneficial effects in the heart. Here, we aim to provide a conceptual framework to explain the broad mode of action of LXRs and how LXR signaling may be an important local and systemic target for the treatment of heart failure. We discuss the potential role of LXRs in systemic conditions associated with heart failure, such as hypertension, diabetes, and renal and vascular disease. Further, we expound on recent data that implicate a direct role for LXR activation in the heart, for its impact on cardiomyocyte damage and loss due to ischemia, and effects on cardiac hypertrophy, fibrosis, and myocardial metabolism. Taken together, the accumulating evidence supports the notion that LXRs may represent a novel therapeutic target for the treatment of heart failure.
      datePublished:2015-11-26T00:00:00Z
      dateModified:2015-11-26T00:00:00Z
      pageStart:1
      pageEnd:17
      license:http://creativecommons.org/licenses/by/4.0/
      sameAs:https://doi.org/10.1007/s00395-015-0520-7
      keywords:
         Cardiac remodeling
         Cardiovascular risk factors
         Heart failure
         Hypertrophy
         Liver X receptors
         Metabolism
         Cardiology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-015-0520-7/MediaObjects/395_2015_520_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-015-0520-7/MediaObjects/395_2015_520_Fig2_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00395-015-0520-7/MediaObjects/395_2015_520_Fig3_HTML.gif
      isPartOf:
         name:Basic Research in Cardiology
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         volumeNumber:111
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      publisher:
         name:Springer Berlin Heidelberg
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      author:
            name:Megan V. Cannon
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            name:Wiek H. van Gilst
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                  name:University of Groningen, University Medical Center Groningen
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                     name:Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
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            address:
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               type:PostalAddress
            type:Organization
      name:Wiek H. van Gilst
      affiliation:
            name:University of Groningen, University Medical Center Groningen
            address:
               name:Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
               type:PostalAddress
            type:Organization
      name:Rudolf A. de Boer
      affiliation:
            name:University of Groningen, University Medical Center Groningen
            address:
               name:Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
      name:Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
      name:Department of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands

External Links {🔗}(698)

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CDN Services {📦}

  • Crossref

8.11s.