Evidence map›Paper›PMID 28921056›Full record

ReviewCurrent atherosclerosis reports2017

Oxidative Stress in Atherosclerosis.

Ajoe John Kattoor, Naga Venkata K Pothineni, Deepak Palagiri, Jawahar L Mehta

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05037604 (Factors Associated With Dermatoporosis), which is not on this map. Cited by 661 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
661citing papers in PubMed, 1 pooled it
28.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT05037604 completednot on this mapstarted 2018, after this paper: background citation

Factors Associated With Dermatoporosis

TypeobservationalSponsorUniversidad Autonoma de San Luis PotosíRan2018 to 2019Enrolled315ConditionsSenile PurpuraArmsQuestionnaire about associated factors, Self questionnaire diagnostic tool, Physical Examination
3 · Its place in the literature

Who cites it

661 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,218 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Review
  7. Na/K-ATPase Signaling in Adipocytes Promotes Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Vascular mechanical forces and vascular diseases.Journal of advanced research · 2026
    Review
  19. Review
  20. Review

601 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Ajoe John KattoorCardiovascular Division, Central Arkansas Veterans Healthcare System and the University of Arkansas for Medical Sciences, Little Rock, AR, 72212, USA.
Naga Venkata K PothineniCardiovascular Division, Central Arkansas Veterans Healthcare System and the University of Arkansas for Medical Sciences, Little Rock, AR, 72212, USA.
Deepak PalagiriCardiovascular Division, Central Arkansas Veterans Healthcare System and the University of Arkansas for Medical Sciences, Little Rock, AR, 72212, USA.
Jawahar L MehtaCardiovascular Division, Central Arkansas Veterans Healthcare System and the University of Arkansas for Medical Sciences, Little Rock, AR, 72212, USA. MehtaJL@uams.edu.
Central Arkansas Veterans Healthcare System · USUniversity of Arkansas for Medical Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewAtherosclerosis is now considered a chronic inflammatory disease. Oxidative stress induced by generation of excess reactive oxygen species has emerged as a critical, final common mechanism in atherosclerosis. Reactive oxygen species (ROS) are a group of small reactive molecules that play critical roles in the regulation of various cell functions and biological processes. Although essential for vascular homeostasis, uncontrolled production of ROS is implicated in vascular injury. Endogenous anti-oxidants function as checkpoints to avoid these untoward consequences of ROS, and an imbalance in the oxidant/anti-oxidant mechanisms leads to a state of oxidative stress. In this review, we discuss the role of ROS and anti-oxidant mechanisms in the development and progression of atherosclerosis, the role of oxidized low-density lipoprotein cholesterol, and highlight potential anti-oxidant therapeutic strategies relevant to atherosclerosis. RECENT

findingsThere is growing evidence on how traditional risk factors translate into oxidative stress and contribute to atherosclerosis. Clinical trials evaluating anti-oxidant supplements had failed to improve atherosclerosis. Current studies focus on newer ROS scavengers that specifically target mitochondrial ROS, newer nanotechnology-based drug delivery systems, gene therapies, and anti-miRNAs. Synthetic LOX-1 modulators that inhibit the effects of Ox-LDL are currently in development. Research over the past few decades has led to identification of multiple ROS generating systems that could potentially be modulated in atherosclerosis. Therapeutic approaches currently being used for atheroslcerotic vascular disease such as aspirin, statins, and renin-angiotensin system inhibitors exert a pleiotropic antioxidative effects. There is ongoing research to identify novel therapeutic modalities to selectively target oxidative stress in atherosclerosis.

Indexed as

AntioxidantsAtherosclerosisHumansLipoproteins, LDLOxidative StressReactive Oxygen SpeciesAntioxidantsLipoproteins, LDLoxidized low density lipoproteinReactive Oxygen SpeciesAnti-oxidantsAtherosclerosisLOX-1Oxidative stressOxLDLReactive oxygen species

Identifiers

PMID28921056
OpenAlexW2755249976

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.