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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/s00018-013-1289-1, but it redirected us to https://link.springer.com/article/10.1007/s00018-013-1289-1. The analysis below is for the second page.

Title[redir]:
Inflammation and immune system interactions in atherosclerosis | Cellular and Molecular Life Sciences
Description:
Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall. Today’s picture is far more complex. Atherosclerosis is considered a chronic inflammatory disease that results in the formation of plaques in large and mid-sized arteries. Both cells of the innate and the adaptive immune system play a crucial role in its pathogenesis. By transforming immune cells into pro- and anti-inflammatory chemokine- and cytokine-producing units, and by guiding the interactions between the different immune cells, the immune system decisively influences the propensity of a given plaque to rupture and cause clinical symptoms like myocardial infarction and stroke. In this review, we give an overview on the newest insights in the role of different immune cells and subtypes in atherosclerosis.

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

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 80,486,609 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We're unsure how the site profits.

Not all websites focus on profit; some are designed to educate, connect people, or share useful tools. People create websites for numerous reasons. And this could be one such example. Doi.org might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

google, scholar, pubmed, cas, atherosclerosis, mice, cells, atherosclerotic, van, thromb, biol, arterioscler, vasc, cell, res, dendritic, circulation, immunol, human, macrophage, lesions, med, clin, role, plaque, invest, apolipoprotein, doicirculationaha, development, hansson, doijci, circ, oxidized, immune, expression, macrophages, exp, lipoprotein, interleukin, inflammation, rev, atherogenesis, immunity, doi, nat, receptor, reduces, witztum, ldl, formation,

Topics {✒️}

il-17a/il-17ra axis plays oxidized low-density lipoprotein month download article/chapter low-grade chronic inflammation tuning t-cell proliferation oxidized low-density lipoproteins antigen-presenting dendritic cells t-cell priming efficacy monoclonal t-cell proliferation mfg-e8-mediated uptake bone marrow-derived cells receptor-mediated lipid uptake partially l-selectin dependent cd4 t-cell-ablated deficient cd40-traf6 signaling macrophage colony-stimulating factor apolipoprotein e-deficient mouse local immune-inflammatory reactions cd8 t-cell migration il-17r signaling disruption apolipoprotein e-deficient mice atp-binding cassette transporters macrophage-mediated proteolytic remodeling immune system deficiency low-density lipoproteins ldl receptor-deficient mice atherosclerotic plaque micro-environment proatherogenic immune responses ifn-gamma potentiates atherosclerosis ldl receptor-null mice apolipoprotein e-knockout mice dendritic cells pulsed cd1d-restricted natural killer th17/treg functional imbalance cd40/cd40l system immune system interactions age-accelerated atherosclerosis correlates monocyte-endothelial cell interactions tgf-beta escape control anti-anti-idiotype antibodies van wanrooij ej modulates plaque composition endoplasmic reticulum stress endoplasmic reticulum stress smooth muscle cells cd1d-dependent activation acute coronary syndrome atherosclerotic lesion formation alternative m2 macrophages ziegler-heitbrock hw

Questions {❓}

  • Alderman CJ, Bunyard PR, Chain BM, Foreman JC, Leake DS, Katz DR (2002) Effects of oxidised low density lipoprotein on dendritic cells: a possible immunoregulatory component of the atherogenic micro-environment?
  • Gerdes N, Zirlik A (2011) Co-stimulatory molecules in and beyond co-stimulation—tipping the balance in atherosclerosis?
  • Harvey EJ, Ramji DP (2005) Interferon-gamma and atherosclerosis: pro- or anti-atherogenic?
  • Therapeutic strategies targeting inflammation and immunity in atherosclerosis: how to proceed?

Schema {🗺️}

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         headline:Inflammation and immune system interactions in atherosclerosis
         description:Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall. Today’s picture is far more complex. Atherosclerosis is considered a chronic inflammatory disease that results in the formation of plaques in large and mid-sized arteries. Both cells of the innate and the adaptive immune system play a crucial role in its pathogenesis. By transforming immune cells into pro- and anti-inflammatory chemokine- and cytokine-producing units, and by guiding the interactions between the different immune cells, the immune system decisively influences the propensity of a given plaque to rupture and cause clinical symptoms like myocardial infarction and stroke. In this review, we give an overview on the newest insights in the role of different immune cells and subtypes in atherosclerosis.
         datePublished:2013-02-21T00:00:00Z
         dateModified:2013-02-21T00:00:00Z
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      headline:Inflammation and immune system interactions in atherosclerosis
      description:Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall. Today’s picture is far more complex. Atherosclerosis is considered a chronic inflammatory disease that results in the formation of plaques in large and mid-sized arteries. Both cells of the innate and the adaptive immune system play a crucial role in its pathogenesis. By transforming immune cells into pro- and anti-inflammatory chemokine- and cytokine-producing units, and by guiding the interactions between the different immune cells, the immune system decisively influences the propensity of a given plaque to rupture and cause clinical symptoms like myocardial infarction and stroke. In this review, we give an overview on the newest insights in the role of different immune cells and subtypes in atherosclerosis.
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         Biochemistry
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External Links {🔗}(889)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {📦}

  • Crossref

5.89s.