Evidence map›Paper›PMID 30302720›Full record

ReviewSports medicine (Auckland, N.Z.)2018

Oxidative Stress and Inflammation, Key Targets of Atherosclerotic Plaque Progression and Vulnerability: Potential Impact of Physical Activity.

Pauline Mury, Erica N Chirico, Mathilde Mura, Antoine Millon, Emmanuelle Canet-Soulas, Vincent Pialoux

Abstract readReview
PubMed Publisher
In one paragraph

Review in Sports medicine (Auckland, N.Z.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  17. Impaired endothelial function contributes to cardiac dysfunction: role of mitochondrial dynamics.American journal of physiology. Heart and circulatory physiology · 2025
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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

6 authors.

Pauline MuryTeam Vascular Biology and Red Blood Cell, Interuniversity Laboratory of Human Movement Biology, University Claude Bernard Lyon 1, University of Lyon, Faculté de Médecine Lyon Est, 8 Avenue Rockefeller, 69008, Lyon, France.
Erica N ChiricoDepartment of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ, USA.
Mathilde MuraTeam Vascular Biology and Red Blood Cell, Interuniversity Laboratory of Human Movement Biology, University Claude Bernard Lyon 1, University of Lyon, Faculté de Médecine Lyon Est, 8 Avenue Rockefeller, 69008, Lyon, France.
Antoine MillonUniversity of Lyon, University Claude Bernard Lyon 1, CarMeN Laboratory, INSERM U1060, Bron, France.
Emmanuelle Canet-SoulasUniversity of Lyon, University Claude Bernard Lyon 1, CarMeN Laboratory, INSERM U1060, Bron, France.
Vincent PialouxTeam Vascular Biology and Red Blood Cell, Interuniversity Laboratory of Human Movement Biology, University Claude Bernard Lyon 1, University of Lyon, Faculté de Médecine Lyon Est, 8 Avenue Rockefeller, 69008, Lyon, France. vincent.pialoux@univ-lyon1.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis, a complex cardiovascular disease, is a leading cause of mortality and morbidity worldwide. Oxidative stress and inflammation are both involved in the development of atherosclerotic plaque as they increase the biological processes associated with this pathology, such as endothelial dysfunction and macrophage recruitment and adhesion. Atherosclerotic plaque rupture leading to major ischemic events is the result of vulnerable plaque progression, which is a result of the detrimental effect of oxidative stress and inflammation on risk factors for atherosclerotic plaque rupture, such as intraplaque hemorrhage, neovascularization, and fibrous cap thickness. Thus, both are key targets for primary and secondary interventions. It is well recognized that chronic physical activity attenuates oxidative stress in healthy subjects via the improvement of antioxidant enzyme capacities and inflammation via the enhancement of anti-inflammatory molecules. Moreover, it was recently shown that chronic physical activity could decrease oxidative stress and inflammation in atherosclerotic patients. The aim of this review is to summarize the role of oxidative stress and inflammation in atherosclerosis and the results of therapeutic interventions targeting them in both preclinical and clinical studies. The effects of chronic physical activity on these two key processes are then reviewed in vulnerable atherosclerotic plaques in both coronary and carotid arteries.

Indexed as

ExerciseInflammationOxidative StressPlaque, AtheroscleroticDisease ProgressionHumansRisk

Identifiers

PMID30302720

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.