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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
  12. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s00395-015-0491-8.

Title:
Macrophages and immune cells in atherosclerosis: recent advances and novel concepts | Basic Research in Cardiology
Description:
Atherosclerotic lesion-related thrombosis is the major cause of myocardial infarction and stroke, which together constitute the leading cause of mortality worldwide. The inflammatory response is considered as a predominant driving force in atherosclerotic plaque formation, growth and progression towards instability and rupture. Notably, accumulation of macrophages in the intima and emergence of a pro-inflammatory milieu are a characteristic feature of plaque progression, and these processes can be modulated by adaptive immune responses. Recently, novel evidences of onsite proliferation of macrophages in lesions and transdifferentiation of smooth muscle cells to macrophages have challenged the prevalent paradigm that macrophage accumulation mostly relies on recruitment of circulating monocytes to plaques. Furthermore, previously unrecognized roles of inflammatory cell subsets such as plasmacytoid dendritic cells, innate response activator B cells or CD8+ T cells in atherosclerosis have emerged, as well as novel mechanisms by which regulatory T cells or natural killer T cells contribute to lesion formation. Here, we review and discuss these recent advances in our understanding of inflammatory processes in atherosclerosis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • 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.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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

We can't see how the site brings in money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

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Topics {✒️}

month download article/chapter follicular t-helper cells granzyme b-dependent cytotoxicity ccl17–ccr4-mediated attraction nkt cell-licensed dcs tuning t-cell proliferation alpha-galactosylceramide rapidly induces apolipoprotein e-deficient mice article basic research single-cell immune landscape smooth muscle cells plasmacytoid dendritic cells hematopoietic progenitor cells full article pdf immune system interactions ait-oufella article cochain cxcl4-induced plaque macrophages alma zernecke privacy choices/manage cookies related subjects cells promotes hypercholesterolemia apoe-deficient mice chemokine receptor axes cd1d-restricted antigens foxp3+ regulatory monocyte/macrophage lineage cell depletion reduces cell turnover characterizes reduces necrotic cores human atherosclerotic plaques pro-inflammatory milieu cd1d-dependent activation monocyte-predisposed hierarchy postnatal murine aorta helper-1 adaptive immunity activate nk cells rauch pj atherosclerotic lesion formation sage ap decreased lesion formation vulnerable atherosclerotic plaques inflammatory cell subsets cell depletion ameliorates european economic area predominant driving force inducible costimulatory molecule von zur muhlen von wnuck lipinski increases igm deposits

Schema {🗺️}

WebPage:
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         headline:Macrophages and immune cells in atherosclerosis: recent advances and novel concepts
         description:Atherosclerotic lesion-related thrombosis is the major cause of myocardial infarction and stroke, which together constitute the leading cause of mortality worldwide. The inflammatory response is considered as a predominant driving force in atherosclerotic plaque formation, growth and progression towards instability and rupture. Notably, accumulation of macrophages in the intima and emergence of a pro-inflammatory milieu are a characteristic feature of plaque progression, and these processes can be modulated by adaptive immune responses. Recently, novel evidences of onsite proliferation of macrophages in lesions and transdifferentiation of smooth muscle cells to macrophages have challenged the prevalent paradigm that macrophage accumulation mostly relies on recruitment of circulating monocytes to plaques. Furthermore, previously unrecognized roles of inflammatory cell subsets such as plasmacytoid dendritic cells, innate response activator B cells or CD8+ T cells in atherosclerosis have emerged, as well as novel mechanisms by which regulatory T cells or natural killer T cells contribute to lesion formation. Here, we review and discuss these recent advances in our understanding of inflammatory processes in atherosclerosis.
         datePublished:2015-05-07T00:00:00Z
         dateModified:2015-05-07T00:00:00Z
         pageStart:1
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         sameAs:https://doi.org/10.1007/s00395-015-0491-8
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            Inflammation
            Immunity
            Macrophages
            T cells
            Vascular smooth muscle cells
            Cardiology
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      headline:Macrophages and immune cells in atherosclerosis: recent advances and novel concepts
      description:Atherosclerotic lesion-related thrombosis is the major cause of myocardial infarction and stroke, which together constitute the leading cause of mortality worldwide. The inflammatory response is considered as a predominant driving force in atherosclerotic plaque formation, growth and progression towards instability and rupture. Notably, accumulation of macrophages in the intima and emergence of a pro-inflammatory milieu are a characteristic feature of plaque progression, and these processes can be modulated by adaptive immune responses. Recently, novel evidences of onsite proliferation of macrophages in lesions and transdifferentiation of smooth muscle cells to macrophages have challenged the prevalent paradigm that macrophage accumulation mostly relies on recruitment of circulating monocytes to plaques. Furthermore, previously unrecognized roles of inflammatory cell subsets such as plasmacytoid dendritic cells, innate response activator B cells or CD8+ T cells in atherosclerosis have emerged, as well as novel mechanisms by which regulatory T cells or natural killer T cells contribute to lesion formation. Here, we review and discuss these recent advances in our understanding of inflammatory processes in atherosclerosis.
      datePublished:2015-05-07T00:00:00Z
      dateModified:2015-05-07T00:00:00Z
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         Inflammation
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         Vascular smooth muscle cells
         Cardiology
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            address:
               name:Institute of Clinical Biochemistry and Pathobiochemistry, University Hospital Würzburg, Würzburg, Germany
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External Links {🔗}(390)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

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