Evidence map›Paper›PMID 37891918›Full record

ReviewAntioxidants (Basel, Switzerland)2023

Protein Carbonylation as a Biomarker of Oxidative Stress and a Therapeutic Target in Neonatal Brain Damage.

José Martínez-Orgado, María Martínez-Vega, Laura Silva, Angela Romero, María de Hoz-Rivera, María Villa, Aarón Del Pozo

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

José Martínez-OrgadoBiomedical Research Foundation, Hospital Clínico San Carlos-IdISSC, 28040 Madrid, Spain.ORCID 0000-0003-4405-3545
María Martínez-VegaBiomedical Research Foundation, Hospital Clínico San Carlos-IdISSC, 28040 Madrid, Spain.
Laura SilvaBiomedical Research Foundation, Hospital Clínico San Carlos-IdISSC, 28040 Madrid, Spain.
Angela RomeroBiomedical Research Foundation, Hospital Clínico San Carlos-IdISSC, 28040 Madrid, Spain.
María de Hoz-RiveraBiomedical Research Foundation, Hospital Clínico San Carlos-IdISSC, 28040 Madrid, Spain.ORCID 0000-0001-5748-6054
María VillaBiomedical Research Foundation, Hospital Clínico San Carlos-IdISSC, 28040 Madrid, Spain.ORCID 0000-0001-9394-4323
Aarón Del PozoBiomedical Research Foundation, Hospital Clínico San Carlos-IdISSC, 28040 Madrid, Spain.
Hospital Clínico San Carlos · ES

Funding

Instituto de Salud Carlos III PI19/00927Instituto de Salud Carlos III RD21/0012/0023
6 · The paper itself

Abstract

Oxidative stress (OS) constitutes a pivotal factor within the mechanisms underlying brain damage, for which the immature brain is particularly vulnerable. This vulnerability is caused by the abundance of immature oligodendrocytes in the immature brain, which are highly susceptible to OS-induced harm. Consequently, any injurious process involving OS within the immature brain can lead to long-term myelination impairment. Among the detrimental repercussions of OS, protein carbonylation stands out as a prominently deleterious consequence. Noteworthy elevation of protein carbonylation is observable across diverse models of neonatal brain injury, following both diffuse and focal hypoxic-ischemic insults, as well as intraventricular hemorrhage, in diverse animal species encompassing rodents and larger mammals, and at varying stages of brain development. In the immature brain, protein carbonylation manifests as a byproduct of reactive nitrogen species, bearing profound implications for cell injury, particularly in terms of inflammation amplification. Moreover, protein carbonylation appears as a therapeutic target for mitigating neonatal brain damage. The administration of a potent antioxidant, such as cannabidiol, yields substantial neuroprotective effects. These encompass the reduction in cerebral damage, restoration of neurobehavioral performance, and preservation of physiological myelination. Such effects are linked to the modulation of protein carbonylation. The assessment of protein carbonylation emerges as a reliable method for comprehending the intricate mechanisms underpinning damage and neuroprotection within neonatal brain injury.

Indexed as

brain damagecannabidiolnewbornoxidative stressprotein carbonylationtranslational models

Identifiers

PMID37891918
PMCPMC10603858
OpenAlexW4387501212

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.