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  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
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We are analyzing https://link.springer.com/article/10.1186/s13045-014-0080-6.

Title:
Immunosuppressive/anti-inflammatory cytokines directly and indirectly inhibit endothelial dysfunction- a novel mechanism for maintaining vascular function | Journal of Hematology & Oncology
Description:
Endothelial dysfunction is a pathological status of the vascular system, which can be broadly defined as an imbalance between endothelium-dependent vasoconstriction and vasodilation. Endothelial dysfunction is a key event in the progression of many pathological processes including atherosclerosis, type II diabetes and hypertension. Previous reports have demonstrated that pro-inflammatory/immunoeffector cytokines significantly promote endothelial dysfunction while numerous novel anti-inflammatory/immunosuppressive cytokines have recently been identified such as interleukin (IL)-35. However, the effects of anti-inflammatory cytokines on endothelial dysfunction have received much less attention. In this analytical review, we focus on the recent progress attained in characterizing the direct and indirect effects of anti-inflammatory/immunosuppressive cytokines in the inhibition of endothelial dysfunction. Our analyses are not only limited to the importance of endothelial dysfunction in cardiovascular disease progression, but also expand into the molecular mechanisms and pathways underlying the inhibition of endothelial dysfunction by anti-inflammatory/immunosuppressive cytokines. Our review suggests that anti-inflammatory/immunosuppressive cytokines serve as novel therapeutic targets for inhibiting endothelial dysfunction, vascular inflammation and cardio- and cerebro-vascular diseases.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Health & Fitness
  • Science

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 7,603,724 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We see no obvious way the site makes 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. Link.springer.com could be secretly minting cash, but we can't detect the process.

Keywords {πŸ”}

pubmed, google, scholar, cas, endothelial, vascular, cells, dysfunction, central, cytokines, expression, enos, function, production, antiinflammatory, role, mice, tgfΞ², interleukin, cytokine, pathway, physiol, activation, cell, inflammatory, human, res, effects, proinflammatory, channels, activity, yang, endotheliumdependent, inflammation, factor, nitric, receptor, ang, circ, cardiovascular, diseases, blood, addition, arteries, oxide, phosphorylation, wang, edhf, artery, endotheliumderived,

Topics {βœ’οΈ}

transforming growth factor-beta immunosuppressive/anti-inflammatory cytokines directly anti-inflammatory/immunosuppressive cytokines serve transforming growth factor-Ξ² anti-inflammatory/immunosuppressive cytokine generated nuclear factor-kappab-dependent induction phosphoinoside 3-kinase-akt-dependent pathway mir-125a/b-5p anti-inflammatory/anti-atherogenic micrornas [169] tumor necrosis factor-Ξ± endothelium-derived hyperpolarizing factor nitric oxide-mediated modulation angiotensin ii-infused mice il-1beta-induced inflammatory response tnf-Ξ±-treated mouse models gm-csf-induced p47phox phosphorylation tnf-Ξ±-infused il-10-/- mice angiotensin-ii-treated mice endothelium-derived hyperpolarizing factors regulating endothelium-dependent vasorelaxation anti-inflammatory cytokines determines tgf-Ξ²/smad2 signaling cytokine anta-gonists include angiotensin-induced vascular injury c-terminal reductase domain nitric oxide synthase responsive anti-inflammatory cytokine anti-inflammatory/immunosuppressive cytokines including lymphocyte-generated lymphokines distinct receptor-derived signals nf-kappab-dependent induction classical anti-inflammatory cytokines categorizing anti-inflammatory cytokines alleviates aldosterone-induced impairment n-terminal oxygenase domain flow-mediated dilation test ang ii-induced development anti-inflammatory cytokine interleukin-10 counteract pro-inflammatory cytokines interleukin-10-induced gene expression anti-inflammatory cytokines protect cytochrome p-450-related edhf anti-inflammatory cytokine levels nitric oxide regulates endothelium-dependent relaxations nf-kb-responsive genes isoforms including tgf-Ξ²1 vehicle-treat control mice /pi3-kinase/akt pathway [51] phosphatidylinositide 3-kinase/akt pathway

Questions {❓}

  • Haddad JJ, Fahlman CS: Redox- and oxidant-mediated regulation of interleukin-10: an anti-inflammatory, antioxidant cytokine?
  • Moussion C, Ortega N, Girard JP: The IL-1-like cytokine IL-33 is constitutively expressed in the nucleus of endothelial cells and epithelial cells in vivo: a novel 'alarmin'?
  • Stenvinkel P: Endothelial dysfunction and inflammation-is there a link?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Immunosuppressive/anti-inflammatory cytokines directly and indirectly inhibit endothelial dysfunction- a novel mechanism for maintaining vascular function
         description:Endothelial dysfunction is a pathological status of the vascular system, which can be broadly defined as an imbalance between endothelium-dependent vasoconstriction and vasodilation. Endothelial dysfunction is a key event in the progression of many pathological processes including atherosclerosis, type II diabetes and hypertension. Previous reports have demonstrated that pro-inflammatory/immunoeffector cytokines significantly promote endothelial dysfunction while numerous novel anti-inflammatory/immunosuppressive cytokines have recently been identified such as interleukin (IL)-35. However, the effects of anti-inflammatory cytokines on endothelial dysfunction have received much less attention. In this analytical review, we focus on the recent progress attained in characterizing the direct and indirect effects of anti-inflammatory/immunosuppressive cytokines in the inhibition of endothelial dysfunction. Our analyses are not only limited to the importance of endothelial dysfunction in cardiovascular disease progression, but also expand into the molecular mechanisms and pathways underlying the inhibition of endothelial dysfunction by anti-inflammatory/immunosuppressive cytokines. Our review suggests that anti-inflammatory/immunosuppressive cytokines serve as novel therapeutic targets for inhibiting endothelial dysfunction, vascular inflammation and cardio- and cerebro-vascular diseases.
         datePublished:2014-10-31T00:00:00Z
         dateModified:2014-10-31T00:00:00Z
         pageStart:1
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            Anti-inflammatory cytokines
            Endothelial dysfunction
            Metabolic cardiovascular diseases
            Oncology
            Hematology
            Cancer Research
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      headline:Immunosuppressive/anti-inflammatory cytokines directly and indirectly inhibit endothelial dysfunction- a novel mechanism for maintaining vascular function
      description:Endothelial dysfunction is a pathological status of the vascular system, which can be broadly defined as an imbalance between endothelium-dependent vasoconstriction and vasodilation. Endothelial dysfunction is a key event in the progression of many pathological processes including atherosclerosis, type II diabetes and hypertension. Previous reports have demonstrated that pro-inflammatory/immunoeffector cytokines significantly promote endothelial dysfunction while numerous novel anti-inflammatory/immunosuppressive cytokines have recently been identified such as interleukin (IL)-35. However, the effects of anti-inflammatory cytokines on endothelial dysfunction have received much less attention. In this analytical review, we focus on the recent progress attained in characterizing the direct and indirect effects of anti-inflammatory/immunosuppressive cytokines in the inhibition of endothelial dysfunction. Our analyses are not only limited to the importance of endothelial dysfunction in cardiovascular disease progression, but also expand into the molecular mechanisms and pathways underlying the inhibition of endothelial dysfunction by anti-inflammatory/immunosuppressive cytokines. Our review suggests that anti-inflammatory/immunosuppressive cytokines serve as novel therapeutic targets for inhibiting endothelial dysfunction, vascular inflammation and cardio- and cerebro-vascular diseases.
      datePublished:2014-10-31T00:00:00Z
      dateModified:2014-10-31T00:00:00Z
      pageStart:1
      pageEnd:14
      license:https://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s13045-014-0080-6
      keywords:
         Anti-inflammatory cytokines
         Endothelial dysfunction
         Metabolic cardiovascular diseases
         Oncology
         Hematology
         Cancer Research
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         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2Fs13045-014-0080-6/MediaObjects/13045_2014_Article_80_Fig1_HTML.jpg
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               type:PostalAddress
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               type:PostalAddress
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      name:Hong Wang
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            name:Temple University School of Medicine
            address:
               name:Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, USA
               type:PostalAddress
            type:Organization
      name:Xiao-feng Yang
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            name:Temple University School of Medicine
            address:
               name:Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, USA
               type:PostalAddress
            type:Organization
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               name:Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, USA
               type:PostalAddress
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      email:[email protected]
PostalAddress:
      name:Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, USA
      name:Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, USA
      name:Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, USA
      name:Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, USA
      name:Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, USA
      name:Department of Pharmacology, Center for Metabolic Disease Research and Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, USA
      name:Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, USA

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