Evidence map›Paper›PMID 22356734›Full record

ArticleAntioxidants & redox signaling2012

Transgenic overexpression of peroxiredoxin-2 attenuates ischemic neuronal injury via suppression of a redox-sensitive pro-death signaling pathway.

Yu Gan, Xunming Ji, Xiaoming Hu, Yumin Luo, Lili Zhang, Peiying Li, Xiangrong Liu, Feng Yan, Peter Vosler, Yanqin Gao and 2 more

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 79 citations in OpenAlex.

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  6. Nrf2 Plays a Key Role in Erythropoiesis during Aging.Antioxidants (Basel, Switzerland) · 2024
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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

12 authors at 1 institution in 1 country.

Yu GanDepartment of Neurosurgery and Cerebrovascular Diseases Research Institute, Xuanwu Hospital, Capital Medical University, Beijing, China.
Xunming Ji
Xiaoming Hu
Yumin Luo
Lili Zhang
Peiying Li
Xiangrong Liu
Feng Yan
Peter Vosler
Yanqin Gao
R Anne Stetler
Jun Chen
Capital Medical University · CN

Funding

INDUCIBLE DNA REPAIR IN CEREBRAL ISCHEMIAR01NS036736 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BENNETT, MICHAEL V L, GRAHAM, STEVEN H · 1997 to 2021
$5.4M
Neuroprotection in Models of Cerebral IschemiaR01NS045048 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2003 to 2015
$3.1M
Neuroprotection Against Parkinsonian Cell DeathR01NS062157 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2010 to 2014
$1.5M
Neuroprotective effect of HSP27 in Cerebral IschemiaR01NS056118 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2006 to 2010
$1.5M
Programmed Cell Death Induced by Cerebral IschemiaR01NS043802 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2002 to 2006
$1.4M
NINDS NIH HHS NS036736NINDS NIH HHS NS043802NINDS NIH HHS NS045048NINDS NIH HHS R01 NS036736NINDS NIH HHS R01 NS045048NINDS NIH HHS R01 NS056118NINDS NIH HHS R01 NS062157
6 · The paper itself

Abstract

aimsPeroxiredoxins (PRXs) are a newly characterized family of peroxide scavenging enzymes that not only help maintain cellular redox homeostasis but also may directly engage in a variety of intracellular signaling pathways. PRX2 is a neuronal-specific PRX believed to participate in cerebral antioxidant responses in several neurodegenerative diseases. This study investigates the potential neuroprotective effect and the underlying mechanism of PRX2 in models of ischemic neuronal injury.

resultsTransgenic mice overexpressing PRX2 showed reduced brain injury and improved neurological recovery up to 3 weeks after transient focal cerebral ischemia compared to wild-type littermates. In primary cultures of cortical neurons, transfection of PRX2 but not the loss-of-catalytic-site PRX2 mutant conferred neuroprotection against cell death induced by oxygen glucose deprivation. PRX2 exhibited potent pro-survival effects in ischemic neurons by maintaining thioredoxin (Trx) in its reduced state, thereby preventing oxidative stress-mediated activation of apoptosis signal-regulating kinase 1 (ASK1) and the downstream MKK/JNK pro-death signaling pathway. PRX2 failed to provide additional neuroprotection against ischemic injury in Trx- or ASK1-knockdown neuron cultures and in mice treated with a JNK inhibitor. INNOVATION: This study provides evidence that neuronal overexpression of PRX2 confers prolonged neuroprotection against ischemic/reperfusion brain injury. Moreover, the results suggest a signaling pathway by which PRX2 suppresses ischemia-induced neuronal apoptosis.

conclusionsEnhanced neuronal expression and activity of PRX2 protect against ischemic neuronal injury by directly modulating the redox-sensitive Trx-ASK1 signaling complex.

Indexed as

Cell DeathSignal TransductionAnimalsBrain IschemiaCatalytic DomainCells, CulturedMaleMiceMice, TransgenicNeuronsPeroxiredoxinsPeroxiredoxins

Identifiers

PMID22356734
PMCPMC3387778
OpenAlexW2021228404

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.