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

We are analyzing https://link.springer.com/article/10.1007/s00125-008-1060-6.

Title:
The HMG-CoA reductase inhibitor rosuvastatin and the angiotensin receptor antagonist candesartan attenuate atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes via effects on advanced glycation, oxidative stress and inflammation | Diabetologia
Description:
Aims/hypothesis We evaluated the anti-atherosclerotic effect of the 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, rosuvastatin, and the angiotensin II receptor blocker (ARB), candesartan, alone and in combination, in the streptozotocin-induced diabetic apolipoprotein E-deficient (Apoe −/−) mouse. Methods Control and streptozotocin-induced diabetic Apoe −/− mice received rosuvastatin (5 mg kg−1 day−1), candesartan (2.5 mg kg−1 day−1), dual therapy or no treatment for 20 weeks. Aortic plaque deposition was assessed by Sudan IV staining and subsequent visual quantification. The abundance of proteins was measured using immunohistochemistry. Results Diabetes was associated with a fourfold increase in total plaque area. Rosuvastatin attenuated plaque area in diabetic mice in the absence of lipid-lowering effects. The anti-atherosclerotic effect of rosuvastatin was comparable to that observed with candesartan. A similar beneficial effect was seen with dual therapy, although it was not superior to monotherapy. Rosuvastatin treatment was associated with attenuated accumulation of AGE and AGE receptor (RAGE) in plaques. Similar beneficial effects on markers of oxidative stress were seen with the ARB and statin. Candesartan was more effective at reducing macrophage accumulation and collagen I abundance in plaques compared with rosuvastatin. The combined effect of candesartan and rosuvastatin was superior in reducing macrophage infiltration, monocyte chemoattractant protein-1 level, vascular AGE accumulation and RAGE abundance in the vascular wall. Furthermore, the combination tended to be more effective in reducing smooth muscle cell infiltration and connective tissue growth factor abundance in plaques. Conclusions/interpretation Rosuvastatin has direct anti-atherosclerotic effects in diabetic macrovascular disease. These effects are independent of effects on lipids and comparable to the effects observed with candesartan.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Social Networks
  • Science

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 7,734,772 visitors per month in the current month.

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How Does Link.springer.com Make Money? {💸}

We can't figure out the monetization strategy.

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 might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

diabetic, rosuvastatin, candesartan, diabetes, mice, effects, google, scholar, plaque, pubmed, cas, control, article, atherosclerosis, wall, effect, treatment, combination, apoe, vascular, fig, abundance, plaques, vessel, angiotensin, effective, area, therapy, study, receptor, table, stress, increase, accumulation, muscle, reduction, oxidative, antiatherosclerotic, age, cell, patients, smooth, increased, nadph, data, rage, treatments, oxidase, model, similar,

Topics {✒️}

diabetes-related end-organ injury membrane-bound nadh-/nadph-oxidases low-density lipoprotein oxidation hyperlipidaemic apolipoprotein e-deficient low-density lipoprotein cholesterol hmg-coa reductase inhibitor cis-acting promoter sequences h-induced lucigenin chemiluminescence c-myc gene expressions hmg-coa reductase inhibitors medical research council smooth muscle cells local renin–angiotensin system angiotensin ii-dependent proliferation back-crossed twenty times pentobarbitone sodium/phenytoin sodium hmg-coa-reductase inhibition renin–angiotensin system plays long-term antecedent glycemia nf-kappab-mediated genes human endothelial cells angiotensin-converting enzyme inhibition anti-atherosclerotic effects conferred renin–angiotensin system contribute randomised placebo-controlled trial monocyte chemoattractant protein-1 angiotensin ii-mediated hypertension anti-atherosclerotic effect conferred high-fat-induced atherosclerosis insulin-dependent diabetes mellitus renin-angiotensin system blockade anti-atherosclerotic effect achieved coronary artery disease pre-clinical setting investigating high-pressure liquid chromatography national heart foundation induces endothelial dysfunction 100 mg/kg body weight cholesterol-dependent oxidative stress direct anti-atherosclerotic effects high-risk diabetic patient simvastatin-dependent plaque stabilization greater anti-atherogenic effect additive anti-oxidative effect altered gene expression human resistance arteries coronary heart disease 3-hydroxy-3-methylglutaryl coa at1 receptor blocker renin–angiotensin system

Questions {❓}

  • Goldberg IJ (2004) Why does diabetes increase atherosclerosis?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:The HMG-CoA reductase inhibitor rosuvastatin and the angiotensin receptor antagonist candesartan attenuate atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes via effects on advanced glycation, oxidative stress and inflammation
         description:We evaluated the anti-atherosclerotic effect of the 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, rosuvastatin, and the angiotensin II receptor blocker (ARB), candesartan, alone and in combination, in the streptozotocin-induced diabetic apolipoprotein E-deficient (Apoe −/−) mouse. Control and streptozotocin-induced diabetic Apoe −/− mice received rosuvastatin (5 mg kg−1 day−1), candesartan (2.5 mg kg−1 day−1), dual therapy or no treatment for 20 weeks. Aortic plaque deposition was assessed by Sudan IV staining and subsequent visual quantification. The abundance of proteins was measured using immunohistochemistry. Diabetes was associated with a fourfold increase in total plaque area. Rosuvastatin attenuated plaque area in diabetic mice in the absence of lipid-lowering effects. The anti-atherosclerotic effect of rosuvastatin was comparable to that observed with candesartan. A similar beneficial effect was seen with dual therapy, although it was not superior to monotherapy. Rosuvastatin treatment was associated with attenuated accumulation of AGE and AGE receptor (RAGE) in plaques. Similar beneficial effects on markers of oxidative stress were seen with the ARB and statin. Candesartan was more effective at reducing macrophage accumulation and collagen I abundance in plaques compared with rosuvastatin. The combined effect of candesartan and rosuvastatin was superior in reducing macrophage infiltration, monocyte chemoattractant protein-1 level, vascular AGE accumulation and RAGE abundance in the vascular wall. Furthermore, the combination tended to be more effective in reducing smooth muscle cell infiltration and connective tissue growth factor abundance in plaques. Rosuvastatin has direct anti-atherosclerotic effects in diabetic macrovascular disease. These effects are independent of effects on lipids and comparable to the effects observed with candesartan.
         datePublished:2008-07-02T00:00:00Z
         dateModified:2008-07-02T00:00:00Z
         pageStart:1731
         pageEnd:1740
         sameAs:https://doi.org/10.1007/s00125-008-1060-6
         keywords:
            Angiotensin II
            Atherosclerosis
            Diabetes
            Diabetic–hypercholesterolaemic mouse
            Statin
            Internal Medicine
            Metabolic Diseases
            Human Physiology
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ScholarlyArticle:
      headline:The HMG-CoA reductase inhibitor rosuvastatin and the angiotensin receptor antagonist candesartan attenuate atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes via effects on advanced glycation, oxidative stress and inflammation
      description:We evaluated the anti-atherosclerotic effect of the 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, rosuvastatin, and the angiotensin II receptor blocker (ARB), candesartan, alone and in combination, in the streptozotocin-induced diabetic apolipoprotein E-deficient (Apoe −/−) mouse. Control and streptozotocin-induced diabetic Apoe −/− mice received rosuvastatin (5 mg kg−1 day−1), candesartan (2.5 mg kg−1 day−1), dual therapy or no treatment for 20 weeks. Aortic plaque deposition was assessed by Sudan IV staining and subsequent visual quantification. The abundance of proteins was measured using immunohistochemistry. Diabetes was associated with a fourfold increase in total plaque area. Rosuvastatin attenuated plaque area in diabetic mice in the absence of lipid-lowering effects. The anti-atherosclerotic effect of rosuvastatin was comparable to that observed with candesartan. A similar beneficial effect was seen with dual therapy, although it was not superior to monotherapy. Rosuvastatin treatment was associated with attenuated accumulation of AGE and AGE receptor (RAGE) in plaques. Similar beneficial effects on markers of oxidative stress were seen with the ARB and statin. Candesartan was more effective at reducing macrophage accumulation and collagen I abundance in plaques compared with rosuvastatin. The combined effect of candesartan and rosuvastatin was superior in reducing macrophage infiltration, monocyte chemoattractant protein-1 level, vascular AGE accumulation and RAGE abundance in the vascular wall. Furthermore, the combination tended to be more effective in reducing smooth muscle cell infiltration and connective tissue growth factor abundance in plaques. Rosuvastatin has direct anti-atherosclerotic effects in diabetic macrovascular disease. These effects are independent of effects on lipids and comparable to the effects observed with candesartan.
      datePublished:2008-07-02T00:00:00Z
      dateModified:2008-07-02T00:00:00Z
      pageStart:1731
      pageEnd:1740
      sameAs:https://doi.org/10.1007/s00125-008-1060-6
      keywords:
         Angiotensin II
         Atherosclerosis
         Diabetes
         Diabetic–hypercholesterolaemic mouse
         Statin
         Internal Medicine
         Metabolic Diseases
         Human Physiology
      image:
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                  name:Baker Heart Research Institute
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                  address:
                     name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
                     type:PostalAddress
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            name:C. Chew
            affiliation:
                  name:Baker Heart Research Institute
                  address:
                     name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
                     type:PostalAddress
                  type:Organization
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            name:V. Boolell
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                  name:Baker Heart Research Institute
                  address:
                     name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
                     type:PostalAddress
                  type:Organization
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            name:Y. S. Rajaram
            affiliation:
                  name:Baker Heart Research Institute
                  address:
                     name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
                     type:PostalAddress
                  type:Organization
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                  address:
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                     type:PostalAddress
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            name:K. A. Jandeleit-Dahm
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                  name:Baker Heart Research Institute
                  address:
                     name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
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         name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
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            name:Baker Heart Research Institute
            address:
               name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
               type:PostalAddress
            type:Organization
      name:S. Giunti
      affiliation:
            name:Baker Heart Research Institute
            address:
               name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
               type:PostalAddress
            type:Organization
      name:K. J. Sheehy
      affiliation:
            name:Baker Heart Research Institute
            address:
               name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
               type:PostalAddress
            type:Organization
      name:C. Chew
      affiliation:
            name:Baker Heart Research Institute
            address:
               name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
               type:PostalAddress
            type:Organization
      name:V. Boolell
      affiliation:
            name:Baker Heart Research Institute
            address:
               name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
               type:PostalAddress
            type:Organization
      name:Y. S. Rajaram
      affiliation:
            name:Baker Heart Research Institute
            address:
               name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
               type:PostalAddress
            type:Organization
      name:M. E. Cooper
      affiliation:
            name:Baker Heart Research Institute
            address:
               name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
               type:PostalAddress
            type:Organization
      name:K. A. Jandeleit-Dahm
      affiliation:
            name:Baker Heart Research Institute
            address:
               name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
      name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
      name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
      name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
      name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
      name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
      name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia
      name:Diabetes Complications Laboratory, Baker Heart Research Institute, Melbourne, Australia

External Links {🔗}(172)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

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