Here's how DOI.ORG makes money* and how much!

*Please read our disclaimer before using our estimates.
Loading...

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/s11010-024-05062-5, but it redirected us to https://link.springer.com/article/10.1007/s11010-024-05062-5. The analysis below is for the second page.

Title[redir]:
Cell death crosstalk in respiratory diseases: unveiling the relationship between pyroptosis and ferroptosis in asthma and COPD | Molecular and Cellular Biochemistry
Description:
Asthma and chronic obstructive pulmonary disease (COPD) are heterogeneous obstructive diseases characterized by airflow limitations and are recognized as significant contributors to fatality all over the globe. Asthma accounts for about 4, 55,000 deaths, and COPD is the 3rd leading contributor of mortality worldwide. The pathogenesis of these two obstructive disorders is complex and involves numerous mechanistic pathways, including inflammation-mediated and non-inflammation-mediated pathways. Among all the pathological categorizations, programmed cell deaths (PCDs) play a dominating role in the progression of these obstructive diseases. The two major PCDs that are involved in structural and functional remodeling in the progression of asthma and COPD are Pyroptosis and Ferroptosis. Pyroptosis is a PCD mechanism mediated by the activation of the Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome, leading to the maturation and release of Interleukin-1β and Interleukin-18, whereas ferroptosis is a lipid peroxidation-associated cell death. In this review, the major molecular pathways contributing to these multifaceted cell deaths have been discussed, and crosstalk among them regarding the pathogenesis of asthma and COPD has been highlighted. Further, the possible therapeutic approaches that can be utilized to mitigate both cell deaths at once have also been illustrated.

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

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?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,420 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Doi.org Make Money? {💸}

We don't see any clear sign of profit-making.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Doi.org has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

pubmed, article, google, scholar, cas, central, cell, ferroptosis, wang, zhang, pyroptosis, chen, asthma, liu, inflammasome, httpsdoiorgs, death, disease, inflammation, nlrp, copd, obstructive, med, cancer, airway, sci, yang, chronic, activation, lung, mol, pulmonary, immunol, cells, role, biol, res, zhao, pathway, epithelial, int, jiang, signaling, nat, zhu, sun, zhou, nature, caspase, pathways,

Topics {✒️}

int/news-room/fact-sheets/detail/chronicobstructive-pulmonary-disease tlr4-nf-κb-myd88 signalling pathway tlr4/myd88/nf-κb pathway tlr4/nf-κb signaling pathway tlr4/nf-kb signaling pathway month download article/chapter ros-mediated nf-κb suppression suppressing tlr-4/nf-κb pathway tlr4/myd88/nf-κb il-13-challenged beas-2b cells cigarette smoke-induced activation modifies lipopolysaccharide-mediated responses sepsis-induced lung injury fatty acid β-oxidation toluene diisocyanate-induced asthma inflammation-related respiratory disease nlrp3-dependent il-1 production ptgs2/pge2 signaling pathway induce il-1β secretion ova-induced asthma model activating nrf2-mediated pathway accepted manuscript version nrf2/ho-1 signaling pathways p53-independent tumor suppression pd-l1-mediated gasdermin ros/nlrp3/caspase-1 pathway aim2 inflammasome-mediated pyroptosis increased il-1β levels resibufogenin suppresses growth short-term mouse model airway smooth muscle cigarette smoke induces birla institute article khawas neelima sharma designed damaged blood-brain barrier full article pdf shigella-induced apoptosis inflammatory signaling pathways acute lung injury inhibiting nf-κb nrf2 signaling pathway activates inflammasome-ferroptosis processes suppressing caspase-4/5/11/gsdmd-mediated attenuates airway inflammation lipid death signals inducing caspase-1-dependent pyroptosis ten hacken nh vanaja sk potential targeted therapies

Questions {❓}

  • Xia X, Wang X, Cheng Z, Qin W, Lei L, Jiang J, Hu J (2019) The role of pyroptosis in cancer: pro-cancer or pro-“host”?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Cell death crosstalk in respiratory diseases: unveiling the relationship between pyroptosis and ferroptosis in asthma and COPD
         description:Asthma and chronic obstructive pulmonary disease (COPD) are heterogeneous obstructive diseases characterized by airflow limitations and are recognized as significant contributors to fatality all over the globe. Asthma accounts for about 4, 55,000 deaths, and COPD is the 3rd leading contributor of mortality worldwide. The pathogenesis of these two obstructive disorders is complex and involves numerous mechanistic pathways, including inflammation-mediated and non-inflammation-mediated pathways. Among all the pathological categorizations, programmed cell deaths (PCDs) play a dominating role in the progression of these obstructive diseases. The two major PCDs that are involved in structural and functional remodeling in the progression of asthma and COPD are Pyroptosis and Ferroptosis. Pyroptosis is a PCD mechanism mediated by the activation of the Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome, leading to the maturation and release of Interleukin-1β and Interleukin-18, whereas ferroptosis is a lipid peroxidation-associated cell death. In this review, the major molecular pathways contributing to these multifaceted cell deaths have been discussed, and crosstalk among them regarding the pathogenesis of asthma and COPD has been highlighted. Further, the possible therapeutic approaches that can be utilized to mitigate both cell deaths at once have also been illustrated.
         datePublished:2024-08-08T00:00:00Z
         dateModified:2024-08-08T00:00:00Z
         pageStart:1305
         pageEnd:1326
         sameAs:https://doi.org/10.1007/s11010-024-05062-5
         keywords:
            Asthma
            COPD
            Pyroptosis
            Ferroptosis
            NLRP3 inflammasome
            Lipid peroxidation
            Biochemistry
            general
            Cardiology
            Cancer Research
            Medical Biochemistry
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig1_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig2_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig3_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig4_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig5_HTML.png
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig6_HTML.png
         isPartOf:
            name:Molecular and Cellular Biochemistry
            issn:
               1573-4919
               0300-8177
            volumeNumber:480
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer US
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Sayak Khawas
               affiliation:
                     name:Birla Institute of Technology
                     address:
                        name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Neelima Sharma
               affiliation:
                     name:Birla Institute of Technology
                     address:
                        name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Cell death crosstalk in respiratory diseases: unveiling the relationship between pyroptosis and ferroptosis in asthma and COPD
      description:Asthma and chronic obstructive pulmonary disease (COPD) are heterogeneous obstructive diseases characterized by airflow limitations and are recognized as significant contributors to fatality all over the globe. Asthma accounts for about 4, 55,000 deaths, and COPD is the 3rd leading contributor of mortality worldwide. The pathogenesis of these two obstructive disorders is complex and involves numerous mechanistic pathways, including inflammation-mediated and non-inflammation-mediated pathways. Among all the pathological categorizations, programmed cell deaths (PCDs) play a dominating role in the progression of these obstructive diseases. The two major PCDs that are involved in structural and functional remodeling in the progression of asthma and COPD are Pyroptosis and Ferroptosis. Pyroptosis is a PCD mechanism mediated by the activation of the Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome, leading to the maturation and release of Interleukin-1β and Interleukin-18, whereas ferroptosis is a lipid peroxidation-associated cell death. In this review, the major molecular pathways contributing to these multifaceted cell deaths have been discussed, and crosstalk among them regarding the pathogenesis of asthma and COPD has been highlighted. Further, the possible therapeutic approaches that can be utilized to mitigate both cell deaths at once have also been illustrated.
      datePublished:2024-08-08T00:00:00Z
      dateModified:2024-08-08T00:00:00Z
      pageStart:1305
      pageEnd:1326
      sameAs:https://doi.org/10.1007/s11010-024-05062-5
      keywords:
         Asthma
         COPD
         Pyroptosis
         Ferroptosis
         NLRP3 inflammasome
         Lipid peroxidation
         Biochemistry
         general
         Cardiology
         Cancer Research
         Medical Biochemistry
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig1_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig2_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig3_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig4_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig5_HTML.png
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11010-024-05062-5/MediaObjects/11010_2024_5062_Fig6_HTML.png
      isPartOf:
         name:Molecular and Cellular Biochemistry
         issn:
            1573-4919
            0300-8177
         volumeNumber:480
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer US
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Sayak Khawas
            affiliation:
                  name:Birla Institute of Technology
                  address:
                     name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Neelima Sharma
            affiliation:
                  name:Birla Institute of Technology
                  address:
                     name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Molecular and Cellular Biochemistry
      issn:
         1573-4919
         0300-8177
      volumeNumber:480
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Birla Institute of Technology
      address:
         name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
         type:PostalAddress
      name:Birla Institute of Technology
      address:
         name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Sayak Khawas
      affiliation:
            name:Birla Institute of Technology
            address:
               name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
               type:PostalAddress
            type:Organization
      name:Neelima Sharma
      affiliation:
            name:Birla Institute of Technology
            address:
               name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
      name:Department of Pharmaceutical Science & Technology, Birla Institute of Technology, Ranchi, India
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(699)

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

5.43s.