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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
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We are analyzing https://link.springer.com/article/10.1007/s10753-022-01751-9.

Title:
Role of T Cells in the Pathogenesis of Rheumatoid Arthritis: Focus on Immunometabolism Dysfunctions | Inflammation
Description:
Evidence demonstrated that metabolic-associated T cell abnormalities could be detected in the early stage of RA development. In this context, molecular evaluations have revealed changes in metabolic pathways, leading to the aggressive phenotype of RA T cells. A growing list of genes is downregulated or upregulated in RA T cells, and most of these genes with abnormal expression fall into the category of metabolic pathways. It has been shown that RA T cells shunt glucose towards the pentose phosphate pathway (PPP), which is associated with a high level of nicotinamide adenine dinucleotide phosphate (NADPH) and intermediate molecules. An increased level of NADPH inhibits ATM activation and thereby increases the proliferation capabilities of the RA T cells. Defects in the DNA repair nuclease MRE11A cause failures in repairing mitochondrial DNA, resulting in inhibiting the fatty acid oxidation pathway and further elevated cytoplasmic lipid droplets. Accumulated lipid droplets employ to generate lipid membranes for the cell building program and are also used to form the front-end membrane ruffles that are accomplices with invasive phenotypes of RA T cells. Metabolic pathway involvement in RA pathogenesis expands the pathogenic concept of the disease beyond the common view of autoimmunity triggered by autoantigen recognition. Increased knowledge about metabolic pathways’ implications in RA pathogenesis paves the way to understand better the environment/gene interactions and host/microbiota interactions and introduce potential therapeutic approaches. This review summarized emerging data about the roles of T cells in RA pathogenesis with a focus on immunometabolism dysfunctions and how these metabolic alterations can affect the disease process.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

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 tell how the site generates income.

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. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

pubmed, article, google, scholar, cas, arthritis, cell, rheumatoid, central, cells, immunology, metabolism, metabolic, research, journal, rheumatology, disease, nature, role, dna, goronzy, sciences, biology, weyand, medicine, lipid, autoimmune, inflammation, pathogenesis, signaling, redox, iran, immunometabolism, review, medical, current, frontiers, effector, reviews, autophagy, karami, molecular, repair, opinion, functions, yang, aging, university, content, activation,

Topics {✒️}

month download article/chapter shahin alizadeh-fanalou anti–citrullinated protein antibodies front-end membrane ruffles costimulatory molecule ligation/blockade mre11–rad50–nbs1 conformations dna double-strand breaks fas-mediated apoptosis contributes mycophenolic acid-mediated suppression acid-sensing ion channels local autoimmune inflammation–lessons treg/th17 cytokine axis full article pdf nuclease mre11a induces article inflammation aims privacy choices/manage cookies article masoumi anticitrullinated protein antibodies reactive oxygen species jafar karami lactate regulates metabolic related subjects stat4 rs7574865 polymorphism tks adaptor proteins additional information publisher' amino acid sensors rheumatology research center elevated dna damage metabolic pathways’ implications scaffold protein tks5 important protein modification central metabolite central hub reactive oxygen homeostasis pentose phosphate pathway dna repair mechanisms central role redox-sensitive signaling coronary artery disease repairing mitochondrial dna host/microbiota interactions indigenous north americans th1/th2 cytokines pathologically expanded peripheral hypoxia-inducible factors host-pathogen interactions thiol chemistry defines premature telomeric loss shahid beheshti hospital sh-af contributed

Schema {🗺️}

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         headline:Role of T Cells in the Pathogenesis of Rheumatoid Arthritis: Focus on Immunometabolism Dysfunctions
         description:Evidence demonstrated that metabolic-associated T cell abnormalities could be detected in the early stage of RA development. In this context, molecular evaluations have revealed changes in metabolic pathways, leading to the aggressive phenotype of RA T cells. A growing list of genes is downregulated or upregulated in RA T cells, and most of these genes with abnormal expression fall into the category of metabolic pathways. It has been shown that RA T cells shunt glucose towards the pentose phosphate pathway (PPP), which is associated with a high level of nicotinamide adenine dinucleotide phosphate (NADPH) and intermediate molecules. An increased level of NADPH inhibits ATM activation and thereby increases the proliferation capabilities of the RA T cells. Defects in the DNA repair nuclease MRE11A cause failures in repairing mitochondrial DNA, resulting in inhibiting the fatty acid oxidation pathway and further elevated cytoplasmic lipid droplets. Accumulated lipid droplets employ to generate lipid membranes for the cell building program and are also used to form the front-end membrane ruffles that are accomplices with invasive phenotypes of RA T cells. Metabolic pathway involvement in RA pathogenesis expands the pathogenic concept of the disease beyond the common view of autoimmunity triggered by autoantigen recognition. Increased knowledge about metabolic pathways’ implications in RA pathogenesis paves the way to understand better the environment/gene interactions and host/microbiota interactions and introduce potential therapeutic approaches. This review summarized emerging data about the roles of T cells in RA pathogenesis with a focus on immunometabolism dysfunctions and how these metabolic alterations can affect the disease process.
         datePublished:2022-10-10T00:00:00Z
         dateModified:2022-10-10T00:00:00Z
         pageStart:88
         pageEnd:102
         sameAs:https://doi.org/10.1007/s10753-022-01751-9
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            RA T cell
            Immunometabolism.
            Immunology
            Rheumatology
            Pharmacology/Toxicology
            Pathology
            Internal Medicine
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      headline:Role of T Cells in the Pathogenesis of Rheumatoid Arthritis: Focus on Immunometabolism Dysfunctions
      description:Evidence demonstrated that metabolic-associated T cell abnormalities could be detected in the early stage of RA development. In this context, molecular evaluations have revealed changes in metabolic pathways, leading to the aggressive phenotype of RA T cells. A growing list of genes is downregulated or upregulated in RA T cells, and most of these genes with abnormal expression fall into the category of metabolic pathways. It has been shown that RA T cells shunt glucose towards the pentose phosphate pathway (PPP), which is associated with a high level of nicotinamide adenine dinucleotide phosphate (NADPH) and intermediate molecules. An increased level of NADPH inhibits ATM activation and thereby increases the proliferation capabilities of the RA T cells. Defects in the DNA repair nuclease MRE11A cause failures in repairing mitochondrial DNA, resulting in inhibiting the fatty acid oxidation pathway and further elevated cytoplasmic lipid droplets. Accumulated lipid droplets employ to generate lipid membranes for the cell building program and are also used to form the front-end membrane ruffles that are accomplices with invasive phenotypes of RA T cells. Metabolic pathway involvement in RA pathogenesis expands the pathogenic concept of the disease beyond the common view of autoimmunity triggered by autoantigen recognition. Increased knowledge about metabolic pathways’ implications in RA pathogenesis paves the way to understand better the environment/gene interactions and host/microbiota interactions and introduce potential therapeutic approaches. This review summarized emerging data about the roles of T cells in RA pathogenesis with a focus on immunometabolism dysfunctions and how these metabolic alterations can affect the disease process.
      datePublished:2022-10-10T00:00:00Z
      dateModified:2022-10-10T00:00:00Z
      pageStart:88
      pageEnd:102
      sameAs:https://doi.org/10.1007/s10753-022-01751-9
      keywords:
         Rheumatoid arthritis
         RA T cell
         Immunometabolism.
         Immunology
         Rheumatology
         Pharmacology/Toxicology
         Pathology
         Internal Medicine
      image:
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                     name:Department of Internal Medicine and Rheumatology, Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
                     type:PostalAddress
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            type:Person
            name:Hossein Khorramdelazad
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         name:Clinical Research and Development Center, Shahid Beheshti Hospital, Qom University of Medical Sciences, Qom, Iran
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      address:
         name:Department of Internal Medicine and Rheumatology, Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
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      name:Iran University of Medical Sciences
      address:
         name:Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
         type:PostalAddress
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      address:
         name:Department of Immunology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
         type:PostalAddress
      name:Semnan University of Medical Sciences
      address:
         name:Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran
         type:PostalAddress
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      address:
         name:Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
         type:PostalAddress
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               name:Clinical Research and Development Center, Shahid Beheshti Hospital, Qom University of Medical Sciences, Qom, Iran
               type:PostalAddress
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      name:Samira Alesaeidi
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            name:Tehran University of Medical Sciences
            address:
               name:Department of Internal Medicine and Rheumatology, Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
               type:PostalAddress
            type:Organization
      name:Hossein Khorramdelazad
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            name:Iran University of Medical Sciences
            address:
               name:Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
               type:PostalAddress
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      name:Mousa Behzadi
      affiliation:
            name:Shahid Beheshti University of Medical Sciences
            address:
               name:Department of Immunology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
               type:PostalAddress
            type:Organization
      name:Rasoul Baharlou
      affiliation:
            name:Semnan University of Medical Sciences
            address:
               name:Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran
               type:PostalAddress
            type:Organization
      name:Shahin Alizadeh-Fanalou
      affiliation:
            name:Iran University of Medical Sciences
            address:
               name:Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Jafar Karami
      affiliation:
            name:Khomein University of Medical Sciences
            address:
               name:Molecular and Medicine Research Center, Khomein University of Medical Sciences, Khomein, Iran
               type:PostalAddress
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      email:[email protected]
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      name:Clinical Research and Development Center, Shahid Beheshti Hospital, Qom University of Medical Sciences, Qom, Iran
      name:Department of Internal Medicine and Rheumatology, Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
      name:Department of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
      name:Department of Immunology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
      name:Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran
      name:Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
      name:Molecular and Medicine Research Center, Khomein University of Medical Sciences, Khomein, Iran
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External Links {🔗}(416)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

4.14s.