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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
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1007/s12016-020-08791-9.

Title:
Anti-inflammatory Action of Statins in Cardiovascular Disease: the Role of Inflammasome and Toll-Like Receptor Pathways | Clinical Reviews in Allergy & Immunology
Description:
Atherosclerosis is one type of cardiovascular disease (CVD) in which activation of the NLRP3 inflammasome and toll-like receptor (TLR) pathways is implicated. One of the most effective treatments for atherosclerosis is the use of statin medications. Recent studies have indicated that statins, in addition to their lipid-lowering effects, exert inhibitory and/or stimulatory effects on the NLRP3 inflammasome and TLRs. Some of the statins lead to activation of the inflammasome and subsequently cause secretion of IL-1β and IL-18. Thus, these actions may further aggravate the disease. On the other hand, some statins cause inhibition of the inflammasome or TLRs and along with lipid-lowering, help to improve the disease by reducing inflammation. In this article, we discuss these contradictory studies and the mechanisms of action of statins on the NLRP3 inflammasome and TLR pathways. The dose-dependent effects of statins on the NLRP3 complex are related to their chemistry, pharmacokinetic properties, and danger signals. Lipophilic statins have more pleiotropic effects on the NLRP3 complex in comparison to hydrophilic statins. Statins can suppress TLR4/MyD88/NF-ĸB signaling and cause an immune response shift to an anti-inflammatory response. Furthermore, statins inhibit the NF-ĸB pathway by decreasing the expression of TLRs 2 and 4. Statins are cost-effective drugs, which should have a continued future in the treatment of atherosclerosis due to both their immune-modulating and lipid-lowering effects.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Health & Fitness
  • Education
  • 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 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 figure out the monetization strategy.

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 {🔍}

pubmed, google, scholar, cas, atherosclerosis, statins, nlrp, tlr, cells, effects, inflammasome, activation, expression, ilβ, receptor, effect, inflammation, patients, inflammatory, levels, central, atorvastatin, role, signaling, cell, atherosclerotic, shown, studies, nfĸb, tlrs, statin, disease, protein, tolllike, pathway, cholesterol, coronary, study, immune, receptors, oxldl, rosuvastatin, endothelial, leads, mice, antiinflammatory, vascular, caspase, cardiovascular, inhibition,

Topics {✒️}

nuclear factor kappa-light-chain-enhancer suppress tlr4/myd88/nf-ĸb signaling suppressing tlr4/myd88/nf-ĸb pathway tlr4/myd88/nf-ĸb signaling pathway 5 mg/day versus 10 mg/day tlr4/myd88/nf-κb signaling 3-hydroxy-3-methylglutaryl-coa reductase tlr4/myd88/nf-ĸb pathway [137] lps-induced nf-ĸb activation hmg-coa reductase inhibitors 3-hydroxy-3-methyl-glutaryl-coenzyme large-scale randomized study bacteria-derived nucleic acids tumor necrosis factor-α nf-kβ transcription factor abolishing tgf-β signaling hmg-coa reductase inhibitor native low-density lipoprotein lipopolysaccharide–induced cytokine production large-species animal model hyperglycemia-induced endothelial dysfunction statin-induced insulin resistance myd88-deficient mice exhibit tight junction–zonula occludens-1 nf-ĸb transcription factor recombinant mouse tgf-β1 suppress nf-ĸb activity apolipoprotein e-deficient mice oxidized low-density lipoprotein affecting p65 nf-ĸb lps-treated animal models lox1-/nf-ĸb pathway mitogen-activated protein kinases renin–angiotensin system blockade stabilizing nf-ĸb inhibitors multiple host-derived molecules called pattern-recognition receptors activates nf-ĸb pathway decreases nf-ĸb activity lps-induced cytokine production nf-κb-dependent induction mitogen-activated protein kinase randomised placebo-controlled trials zeinab deris zayeri monocyte tlr-signaling network major histocompatibility complex-ii c-reactive protein levels pma-stimulated thp-1 monocytes leucine-rich extracellular region suppressed nf-ĸb activity

Questions {❓}

  • Abais JM, Xia M, Zhang Y, Boini KM, Li P-L (2015) Redox regulation of NLRP3 inflammasomes: ROS as trigger or effector?
  • Andreakos E, Foxwell B, Feldmann M (2004) Is targeting Toll-like receptors and their signaling pathway a useful therapeutic approach to modulating cytokine-driven inflammation?
  • Arboix A, García-Eroles L, Oliveres M, Targa C, Balcells M, Massons J (2010) Pretreatment with statins improves early outcome in patients with first-ever ischaemic stroke: a pleiotropic effect of statins or a beneficial effect of hypercholesterolemia?
  • Bielinska A, Gluszko P (2007) Statins-are they potentially useful in rheumatology?
  • Henriksbo BD, Schertzer JD (2015) Is immunity a mechanism contributing to statin-induced diabetes?
  • Nelson CP, Erridge C (2019) Are toll-like receptors potential drug targets for atherosclerosis?
  • Ridker PM (2013) Closing the loop on inflammation and atherothrombosis: why perform the CIRT and CANTOS trials?
  • Sahebkar A, Watts GF (2013) New therapies targeting apoB metabolism for high-risk patients with inherited dyslipidaemias: what can the clinician expect?
  • Schönbeck U, Libby P (2004) Inflammation, immunity, and HMG-CoA reductase inhibitors: statins as antiinflammatory agents?
  • Yuan C, Zhou L, Cheng J, Zhang J, Teng Y, Huang M et al (2012) Statins as potential therapeutic drug for asthma?

Schema {🗺️}

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         headline:Anti-inflammatory Action of Statins in Cardiovascular Disease: the Role of Inflammasome and Toll-Like Receptor Pathways
         description:Atherosclerosis is one type of cardiovascular disease (CVD) in which activation of the NLRP3 inflammasome and toll-like receptor (TLR) pathways is implicated. One of the most effective treatments for atherosclerosis is the use of statin medications. Recent studies have indicated that statins, in addition to their lipid-lowering effects, exert inhibitory and/or stimulatory effects on the NLRP3 inflammasome and TLRs. Some of the statins lead to activation of the inflammasome and subsequently cause secretion of IL-1β and IL-18. Thus, these actions may further aggravate the disease. On the other hand, some statins cause inhibition of the inflammasome or TLRs and along with lipid-lowering, help to improve the disease by reducing inflammation. In this article, we discuss these contradictory studies and the mechanisms of action of statins on the NLRP3 inflammasome and TLR pathways. The dose-dependent effects of statins on the NLRP3 complex are related to their chemistry, pharmacokinetic properties, and danger signals. Lipophilic statins have more pleiotropic effects on the NLRP3 complex in comparison to hydrophilic statins. Statins can suppress TLR4/MyD88/NF-ĸB signaling and cause an immune response shift to an anti-inflammatory response. Furthermore, statins inhibit the NF-ĸB pathway by decreasing the expression of TLRs 2 and 4. Statins are cost-effective drugs, which should have a continued future in the treatment of atherosclerosis due to both their immune-modulating and lipid-lowering effects.
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      headline:Anti-inflammatory Action of Statins in Cardiovascular Disease: the Role of Inflammasome and Toll-Like Receptor Pathways
      description:Atherosclerosis is one type of cardiovascular disease (CVD) in which activation of the NLRP3 inflammasome and toll-like receptor (TLR) pathways is implicated. One of the most effective treatments for atherosclerosis is the use of statin medications. Recent studies have indicated that statins, in addition to their lipid-lowering effects, exert inhibitory and/or stimulatory effects on the NLRP3 inflammasome and TLRs. Some of the statins lead to activation of the inflammasome and subsequently cause secretion of IL-1β and IL-18. Thus, these actions may further aggravate the disease. On the other hand, some statins cause inhibition of the inflammasome or TLRs and along with lipid-lowering, help to improve the disease by reducing inflammation. In this article, we discuss these contradictory studies and the mechanisms of action of statins on the NLRP3 inflammasome and TLR pathways. The dose-dependent effects of statins on the NLRP3 complex are related to their chemistry, pharmacokinetic properties, and danger signals. Lipophilic statins have more pleiotropic effects on the NLRP3 complex in comparison to hydrophilic statins. Statins can suppress TLR4/MyD88/NF-ĸB signaling and cause an immune response shift to an anti-inflammatory response. Furthermore, statins inhibit the NF-ĸB pathway by decreasing the expression of TLRs 2 and 4. Statins are cost-effective drugs, which should have a continued future in the treatment of atherosclerosis due to both their immune-modulating and lipid-lowering effects.
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         NLRP3
         Inflammasome
         TLR4
         TLR2
         Cardiovascular disease
         Atherosclerosis
         Allergology
         Immunology
         Internal Medicine
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            address:
               name:Polish Mother’s Memorial Hospital Research Institute (PMMHRI), Lodz, Poland
               type:PostalAddress
            type:Organization
      name:Khalid Al-Rasadi
      affiliation:
            name:Sultan Qaboos University
            address:
               name:Medical Research Centre, Sultan Qaboos University, Muscat, Oman
               type:PostalAddress
            type:Organization
            name:Sultan Qaboos University
            address:
               name:Department of Biochemistry, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman
               type:PostalAddress
            type:Organization
      name:Thomas P. Johnston
      affiliation:
            name:University of Missouri-Kansas City
            address:
               name:Division of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Missouri-Kansas City, Kansas City, USA
               type:PostalAddress
            type:Organization
      name:Amirhossein Sahebkar
      affiliation:
            name:FDA
            address:
               name:Halal Research Center of IRI, FDA, Tehran, Iran
               type:PostalAddress
            type:Organization
            name:Mashhad University of Medical Sciences
            address:
               name:Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
               type:PostalAddress
            type:Organization
            name:Mashhad University of Medical Sciences
            address:
               name:Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Immunology, Faculty of medicine, Mashhad University of Medical Sciences, Mashhad, Iran
      name:Department of Immunology, Faculty of medicine, Mashhad University of Medical Sciences, Mashhad, Iran
      name:Department of Immunology, Faculty of medicine, Mashhad University of Medical Sciences, Mashhad, Iran
      name:Department of Immunology, Faculty of medicine, Mashhad University of Medical Sciences, Mashhad, Iran
      name:Golestan Hospital Clinical Research Development Unit, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
      name:Mashhad University of Medical Science, Mashhad, Iran
      name:Department of Hypertension, WAM University Hospital in Lodz, Medical University of Lodz, Lodz, Poland
      name:Polish Mother’s Memorial Hospital Research Institute (PMMHRI), Lodz, Poland
      name:Medical Research Centre, Sultan Qaboos University, Muscat, Oman
      name:Department of Biochemistry, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman
      name:Division of Pharmacology and Pharmaceutical Sciences, School of Pharmacy, University of Missouri-Kansas City, Kansas City, USA
      name:Halal Research Center of IRI, FDA, Tehran, Iran
      name:Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
      name:Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

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