Evidence map›Paper›PMID 30042332›Full record

ReviewAntioxidants (Basel, Switzerland)2018

Targeting Oxidative Stress and Mitochondrial Dysfunction in the Treatment of Impaired Wound Healing: A Systematic Review.

Mariola Cano Sanchez, Steve Lancel, Eric Boulanger, Remi Neviere

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 257 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
257citing papers in PubMed, 2 pooled it
28.4field-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.

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

257 citing papers in PubMed, 2 syntheses or guidelines pooled it, 535 citations in OpenAlex.

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197 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 4 institutions in 2 countries.

Mariola Cano SanchezLaboratory of Cardiovascular Physiology, Antilles University, P-97200 Fort de France, France. mariola.cano@uvic.cat.
Steve LancelINSERM U1011-EGID, Institut Pasteur de Lille, Université Lille, CHU Lille, F-59000 Lille, France. slancel@univ-lille2.fr.
Eric BoulangerINSERM U995-LIRIC Inflammation Research International Centre, Université Lille, F-59000 Lille, France. eric.boulanger@univ-lille2.fr.
Remi NeviereLaboratory of Cardiovascular Physiology, Antilles University, P-97200 Fort de France, France. remi.neviere@chu-martinique.fr.
Inserm · FRInstitut Pasteur de Lille · FRLille Inflammation Research International Center · FRUniversitat de Vic - Universitat Central de Catalunya · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wound healing is a well-tuned biological process, which is achieved via consecutive and overlapping phases including hemostasis, inflammatory-related events, cell proliferation and tissue remodeling. Several factors can impair wound healing such as oxygenation defects, aging, and stress as well as deleterious health conditions such as infection, diabetes, alcohol overuse, smoking and impaired nutritional status. Growing evidence suggests that reactive oxygen species (ROS) are crucial regulators of several phases of healing processes. ROS are centrally involved in all wound healing processes as low concentrations of ROS generation are required for the fight against invading microorganisms and cell survival signaling. Excessive production of ROS or impaired ROS detoxification causes oxidative damage, which is the main cause of non-healing chronic wounds. In this context, experimental and clinical studies have revealed that antioxidant and anti-inflammatory strategies have proven beneficial in the non-healing state. Among available antioxidant strategies, treatments using mitochondrial-targeted antioxidants are of particular interest. Specifically, mitochondrial-targeted peptides such as elamipretide have the potential to mitigate mitochondrial dysfunction and aberrant inflammatory response through activation of nucleotide-binding oligomerization domain (NOD)-like family receptors, such as the pyrin domain containing 3 (NLRP3) inflammasome, nuclear factor-kappa B (NF-κB) signaling pathway inhibition, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2).

Indexed as

advanced glycation end productsantioxidantsdiabetesinflammationmitochondriareactive oxygen specieswound healing

Identifiers

PMID30042332
PMCPMC6115926
OpenAlexW2883340199

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.