We are analyzing https://link.springer.com/article/10.1007/s11883-018-0737-7.

Title:
Antioxidants in the Fight Against Atherosclerosis: Is This a Dead End? | Current Atherosclerosis Reports
Description:
Purpose of Review The purpose of this review is to focus on the outcome of recent antioxidant interventions using synthetic and naturally occurring molecules established as adjuvant strategies to lipid-lowering or anti-inflammatory therapies designed to reduce the risk of cardiovascular disease. Recent Findings To date, accumulated evidence regarding oxidation as a pro-atherogenic factor indicates that redox biochemical events involved in atherogenesis are indeed a very attractive target for the management of cardiovascular disease in the clinic. Nevertheless, although evidence indicates that redox reactions are important in the initiation and progression of atherosclerosis, oxidation with a pro-atherogenic context does not eliminate the fact that oxidation participates in many cases as an essential messenger of important cellular signaling pathways. Therefore, disease management and therapeutic goals require not only high-precision and high-sensitivity methods to detect in plasma very low amounts of reducing and oxidizing molecules but also a much better understanding of the normal processes and metabolic pathways influenced and/or controlled by oxidative stress. As several methodologies have been specifically described for the quantification of the total antioxidant capacity and the oxidation state of diverse biological systems, a successful way to carefully study how redox reactions influence atherosclerosis can be achieved. Summary Since there is still a lack of standardization with many of these methods, clinical trials studying antioxidant capacity have been difficult to compare and therefore difficult to use in order to reach a conclusion. We believe a comprehensive analysis of new knowledge and its relationship with the presence of plasma antioxidants and their reducing capacity will undoubtedly open new ways to understand and develop new therapeutic pathways in the fight not only against atherosclerosis but also against other degenerative diseases.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Health & Fitness
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.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

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

We're unsure how the site profits.

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. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

pubmed, article, google, scholar, cas, atherosclerosis, antioxidant, plasma, ldl, oxidation, disease, antioxidants, expression, oxidative, central, coronary, cell, cells, stress, patients, oxidized, vitamin, cholesterol, med, capacity, clinical, lipid, lipoprotein, mice, study, effects, molecules, risk, cardiovascular, plaque, acid, effect, atherosclerotic, presence, heart, development, artery, nutr, studies, present, free, biol, process, metabolism, vascular,

Topics {✒️}

jaime mas-oliva declare article toledo-ibelles jaime mas-oliva low-density lipoprotein oxidation serum high-density lipoprotein article download pdf jl witztum focusing low-serum carotenoid concentrations cholesterol-enriched diet presented transcription factors nf-κβ apolipoprotein e-deficient mice long-term supplementation global health observatory erk1/2-dependent nf-κb pro-atherogenic condition exacerbated ldl receptor-deficient mice int/gho/publications/world_health_statistics/2014 anti-atherogenic metabolic status oxldl-mediated oxidative stress β-carotene negatively correlates cigarette smoke extract oxidation-reduction reactions play anti-inflammatory therapies designed low-density lipoprotein int/gho/data/node aortic intima-media thickness smooth muscle cells high-density lipoprotein high-density lipoprotein low-density lipoproteins lower intima-media thickness diverse oxidation-reduction reactions 6-year post-trial follow pro-atherogenic lipid metabolism vascular damage induced toledo-ibelles open access published high-cardiovascular-risk populations privacy choices/manage cookies carreón-torres je atherogenic stimulus reduces randomized clinical trial acute coronary syndrome widely accepted hypothesis vickers kc oxidized ldl-exposed macrophages noise-stress-induced redox reactions depend apo ai concentrations polyunsaturated fatty acid

Questions {❓}

Antioxidants in the Fight Against Atherosclerosis: Is This a Dead End?
Antioxidants in the Fight Against Atherosclerosis: Is This a Dead End?
CODWORLD?
Does short-term vitamin C reduce cardiovascular risk in type 2 diabetes?
Is the extent of atherosclerosis related to resistance of LDL to oxidation?
ROS in Atherosclerosis: What We Know?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Antioxidants in the Fight Against Atherosclerosis: Is This a Dead End?
         description:The purpose of this review is to focus on the outcome of recent antioxidant interventions using synthetic and naturally occurring molecules established as adjuvant strategies to lipid-lowering or anti-inflammatory therapies designed to reduce the risk of cardiovascular disease. To date, accumulated evidence regarding oxidation as a pro-atherogenic factor indicates that redox biochemical events involved in atherogenesis are indeed a very attractive target for the management of cardiovascular disease in the clinic. Nevertheless, although evidence indicates that redox reactions are important in the initiation and progression of atherosclerosis, oxidation with a pro-atherogenic context does not eliminate the fact that oxidation participates in many cases as an essential messenger of important cellular signaling pathways. Therefore, disease management and therapeutic goals require not only high-precision and high-sensitivity methods to detect in plasma very low amounts of reducing and oxidizing molecules but also a much better understanding of the normal processes and metabolic pathways influenced and/or controlled by oxidative stress. As several methodologies have been specifically described for the quantification of the total antioxidant capacity and the oxidation state of diverse biological systems, a successful way to carefully study how redox reactions influence atherosclerosis can be achieved. Since there is still a lack of standardization with many of these methods, clinical trials studying antioxidant capacity have been difficult to compare and therefore difficult to use in order to reach a conclusion. We believe a comprehensive analysis of new knowledge and its relationship with the presence of plasma antioxidants and their reducing capacity will undoubtedly open new ways to understand and develop new therapeutic pathways in the fight not only against atherosclerosis but also against other degenerative diseases.
         datePublished:2018-05-21T00:00:00Z
         dateModified:2018-05-21T00:00:00Z
         pageStart:1
         pageEnd:12
         sameAs:https://doi.org/10.1007/s11883-018-0737-7
         keywords:
            Atherosclerosis
            Cardiovascular disease
            Antioxidant therapy
            Redox reactions
            Standardization factors
            Angiology
            Cardiology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11883-018-0737-7/MediaObjects/11883_2018_737_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11883-018-0737-7/MediaObjects/11883_2018_737_Fig2_HTML.gif
         isPartOf:
            name:Current Atherosclerosis Reports
            issn:
               1534-6242
               1523-3804
            volumeNumber:20
            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:Paola Toledo-Ibelles
               affiliation:
                     name:Universidad Nacional Autónoma de México
                     address:
                        name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jaime Mas-Oliva
               affiliation:
                     name:Universidad Nacional Autónoma de México
                     address:
                        name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Antioxidants in the Fight Against Atherosclerosis: Is This a Dead End?
      description:The purpose of this review is to focus on the outcome of recent antioxidant interventions using synthetic and naturally occurring molecules established as adjuvant strategies to lipid-lowering or anti-inflammatory therapies designed to reduce the risk of cardiovascular disease. To date, accumulated evidence regarding oxidation as a pro-atherogenic factor indicates that redox biochemical events involved in atherogenesis are indeed a very attractive target for the management of cardiovascular disease in the clinic. Nevertheless, although evidence indicates that redox reactions are important in the initiation and progression of atherosclerosis, oxidation with a pro-atherogenic context does not eliminate the fact that oxidation participates in many cases as an essential messenger of important cellular signaling pathways. Therefore, disease management and therapeutic goals require not only high-precision and high-sensitivity methods to detect in plasma very low amounts of reducing and oxidizing molecules but also a much better understanding of the normal processes and metabolic pathways influenced and/or controlled by oxidative stress. As several methodologies have been specifically described for the quantification of the total antioxidant capacity and the oxidation state of diverse biological systems, a successful way to carefully study how redox reactions influence atherosclerosis can be achieved. Since there is still a lack of standardization with many of these methods, clinical trials studying antioxidant capacity have been difficult to compare and therefore difficult to use in order to reach a conclusion. We believe a comprehensive analysis of new knowledge and its relationship with the presence of plasma antioxidants and their reducing capacity will undoubtedly open new ways to understand and develop new therapeutic pathways in the fight not only against atherosclerosis but also against other degenerative diseases.
      datePublished:2018-05-21T00:00:00Z
      dateModified:2018-05-21T00:00:00Z
      pageStart:1
      pageEnd:12
      sameAs:https://doi.org/10.1007/s11883-018-0737-7
      keywords:
         Atherosclerosis
         Cardiovascular disease
         Antioxidant therapy
         Redox reactions
         Standardization factors
         Angiology
         Cardiology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11883-018-0737-7/MediaObjects/11883_2018_737_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs11883-018-0737-7/MediaObjects/11883_2018_737_Fig2_HTML.gif
      isPartOf:
         name:Current Atherosclerosis Reports
         issn:
            1534-6242
            1523-3804
         volumeNumber:20
         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:Paola Toledo-Ibelles
            affiliation:
                  name:Universidad Nacional Autónoma de México
                  address:
                     name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jaime Mas-Oliva
            affiliation:
                  name:Universidad Nacional Autónoma de México
                  address:
                     name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Current Atherosclerosis Reports
      issn:
         1534-6242
         1523-3804
      volumeNumber:20
Organization:
      name:Springer US
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Universidad Nacional Autónoma de México
      address:
         name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
         type:PostalAddress
      name:Universidad Nacional Autónoma de México
      address:
         name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Paola Toledo-Ibelles
      affiliation:
            name:Universidad Nacional Autónoma de México
            address:
               name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
               type:PostalAddress
            type:Organization
      name:Jaime Mas-Oliva
      affiliation:
            name:Universidad Nacional Autónoma de México
            address:
               name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
      name:Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico

External Links {🔗}(402)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.37s.

LINK . SPRINGER . COM {}