Evidence map›Paper›PMID 12843286›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons.

Jianrong Li, Judith C Lin, Hong Wang, James W Peterson, Barbara C Furie, Bruce Furie, Sara L Booth, Joseph J Volpe, Paul A Rosenberg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 2 pooled it
7.3field-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

105 citing papers in PubMed, 2 syntheses or guidelines pooled it, 242 citations in OpenAlex.

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  15. Antioxidants: a comprehensive review.Archives of toxicology · 2025
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45 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

9 authors at 3 institutions in 1 country.

Jianrong LiDepartment of Neurology, Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.
Judith C Lin
Hong Wang
James W Peterson
Barbara C Furie
Bruce Furie
Sara L Booth
Joseph J Volpe
Paul A Rosenberg
Harvard University · USBeth Israel Deaconess Medical Center · USTufts University · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
PERIVENTRICULAR LEUKOMALACIA IN THE PREMATURE INFANTP01NS038475 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI ROSENBERG, PAUL ALLEN · 2000 to 2009
$13.2M
STRUCTURE OF THE VITAMIN K-DEPENDENT CARBOXYLASEP01HL042443 · NHLBI · TUFTS MEDICAL CENTER · PI FURIE, BARBARA C · 1989 to 2003
$7.4M
NHLBI NIH HHS HL42443NHLBI NIH HHS P01 HL042443NICHD NIH HHS HD18655NICHD NIH HHS P30 HD018655NINDS NIH HHS NS38475NINDS NIH HHS P01 NS038475
6 · The paper itself

Abstract

Oxidative stress is believed to be the cause of cell death in multiple disorders of the brain, including perinatal hypoxia/ischemia. Glutamate, cystine deprivation, homocysteic acid, and the glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to immature neurons and oligodendrocytes by depleting intracellular glutathione. Although vitamin K is not a classical antioxidant, we report here the novel finding that vitamin K1 and K2 (menaquinone-4) potently inhibit glutathione depletion-mediated oxidative cell death in primary cultures of oligodendrocyte precursors and immature fetal cortical neurons with EC50 values of 30 nm and 2 nm, respectively. The mechanism by which vitamin K blocks oxidative injury is independent of its only known biological function as a cofactor for gamma-glutamylcarboxylase, an enzyme responsible for posttranslational modification of specific proteins. Neither oligodendrocytes nor neurons possess significant vitamin K-dependent carboxylase or epoxidase activity. Furthermore, the vitamin K antagonists warfarin and dicoumarol and the direct carboxylase inhibitor 2-chloro-vitamin K1 have no effect on the protective function of vitamin K against oxidative injury. Vitamin K does not prevent the depletion of intracellular glutathione caused by cystine deprivation but completely blocks free radical accumulation and cell death. The protective and potent efficacy of this naturally occurring vitamin, with no established clinical side effects, suggests a potential therapeutic application in preventing oxidative damage to undifferentiated oligodendrocytes in perinatal hypoxic/ischemic brain injury.

Indexed as

AnimalsAntioxidantsCell DeathCells, CulturedCystineDose-Response Relationship, Druggamma-GlutamylcyclotransferaseGlutathioneNeuronsNeuroprotective AgentsOligodendrogliaOxidative StressRatsRats, Sprague-DawleyReactive Oxygen SpeciesStem CellsAntioxidantsCystinegamma-GlutamylcyclotransferaseGlutathionemenatetrenoneNeuroprotective AgentsReactive Oxygen SpeciesVitamin K 1Vitamin K 2

Identifiers

PMID12843286
PMCPMC6741273
OpenAlexW1963423101

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.