Evidence map›Paper›PMID 29964171›Full record

ReviewFree radical biology & medicine2018

Oxidized phospholipid signaling in traumatic brain injury.

Tamil S Anthonymuthu, Elizabeth M Kenny, Andrew M Lamade, Valerian E Kagan, Hülya Bayır

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 89 citations in OpenAlex.

  1. Extracellular Mitochondria Mediate Endothelial Injury After Traumatic Brain Injury.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
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  10. Traumatic brain injury-related ferroptosis: current perspectives.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  11. Prenatal Nitrogen Oxide (NOEnvironmental science & technology · 2025
    Article
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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

5 authors at 1 institution in 2 countries.

Tamil S AnthonymuthuSafar Center for Resuscitation Research, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA 15224, United States; Center for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15261, United States.
Elizabeth M KennySafar Center for Resuscitation Research, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA 15224, United States; Center for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15261, United States.
Andrew M LamadeSafar Center for Resuscitation Research, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA 15224, United States; Center for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15261, United States.
Valerian E KaganCenter for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15261, United States; Laboratory of Navigational Redox Lipidomics in Biomedicine, Department of Human Pathology, IM Sechenov First Moscow State Medical University, Russian Federation.
Hülya BayırSafar Center for Resuscitation Research, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA 15224, United States; Center for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15261, United States; Children's Neuroscience Institute, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, 15224, United States. Electronic address: bayihx@ccm.upmc.edu.
University of Pittsburgh · US

Funding

Training and EducationU19AI068021 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GREENBERGER, JOEL S · 2005 to 2019
$44.4M
Regulation of Cardiolin Byosynthesis in Epithelial InjuryP01HL114453 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2014 to 2023
$21.3M
Mapping Lipid Oxidation in Traumatic Brain Injury by Mass Spectrometric ImagingR01NS076511 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Hülya Bayir, Valerian E Kagan · 2012 to 2026
$6.8M
Lipids and Myeloid Cell Function in CancerR01CA165065 · NCI · WISTAR INSTITUTE · PI KAGAN, VALERIAN E, MONTANER, LUIS J · 2012 to 2022
$3.8M
Oxidative Lipidomics in Pediatric Traumatic Brain InjuryR01NS061817 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BAYIR, HÜLYA · 2008 to 2018
$3.3M
Oxidative Lipidomics in Pediatric Traumatic Brain InjuryR37NS061817 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Hülya Bayir · 2021 to 2026
$2.2M
Mitochondria-Targeted Redox Therapy for Cerebral Ischemia in the Developing BrainR01NS084604 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BAYIR, HÜLYA, CLARK, ROBERT S B · 2014 to 2018
$2.0M
NCI NIH HHS R01 CA165065NHLBI NIH HHS P01 HL114453NIAID NIH HHS U19 AI068021NINDS NIH HHS R01 NS061817NINDS NIH HHS R01 NS076511NINDS NIH HHS R01 NS084604NINDS NIH HHS R37 NS061817
6 · The paper itself

Abstract

Oxidative stress is a major contributor to secondary injury signaling cascades following traumatic brain injury (TBI). The role of lipid peroxidation in the pathophysiology of a traumatic insult to neural tissue is increasingly recognized. As the methods to quantify lipid peroxidation have gradually improved, so has the understanding of mechanistic details of lipid peroxidation and related signaling events in the injury pathogenesis. While free-radical mediated, non-enzymatic lipid peroxidation has long been studied, recent advances in redox lipidomics have demonstrated the significant contribution of enzymatic lipid peroxidation to TBI pathogenesis. Complex interactions between inflammation, phospholipid peroxidation, and hydrolysis define the engagement of different cell death programs and the severity of injury and outcome. This review focuses on enzymatic phospholipid peroxidation after TBI, including the mechanism of production, signaling roles in secondary injury pathology, and temporal course of production with respect to inflammatory response. In light of the newly identified phospholipid oxidation mechanisms, we also discuss possible therapeutic targets to improve neurocognitive outcome after TBI. Finally, we discuss current limitations in identifying oxidized phospholipids and possible methodologic improvements that can offer a deeper insight into the region-specific distribution and subcellular localization of phospholipid oxidation after TBI.

Indexed as

AnimalsBrain Injuries, TraumaticHumansLipid PeroxidationOxidation-ReductionOxidative StressPhospholipidsSignal TransductionPhospholipidsApoptosisEfferocytosisFerroptosisInflammationLipid mediatorRedox lipidomics

Identifiers

PMID29964171
PMCPMC6098726
OpenAlexW2809759170

What OpenQuestion holds

Textmetadata
LicenceTDM
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.