Evidence map›Paper›PMID 23564995›Full record

ArticleSleep2013

C/EBP homologous binding protein (CHOP) underlies neural injury in sleep apnea model.

Yu-Ting Chou, Guanxia Zhan, Yan Zhu, Polina Fenik, Lori Panossian, Yanpeng Li, Jing Zhang, Sigrid Veasey

Open access · bronzeAbstract read
In one paragraph

Article in Sleep, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  13. Hypoxia-inducible factors and obstructive sleep apnea.The Journal of clinical investigation · 2020
    Review
  14. Article
  15. Article
  16. Intermittent Hypoxia Disrupts Adult Neurogenesis and Synaptic Plasticity in the Dentate Gyrus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  17. Review
  18. Review
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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

8 authors at 4 institutions in 4 countries.

Yu-Ting ChouSleep Center, Department of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Chiayi, Taiwan.
Guanxia Zhan
Yan Zhu
Polina Fenik
Lori Panossian
Yanpeng Li
Jing Zhang
Sigrid Veasey
Canadian Sleep & Circadian Network · CAUniversity of Pennsylvania · USChang Gung University of Science and Technology · TWPeking University First Hospital · CN

Funding

Intermittent Hypoxia: Mechanisms of HypersomnolenceR01HL079588 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI VEASEY, SIGRID C · 2006 to 2015
$3.1M
Sleep Fatigue &Cognitive Correlates in Pediatric HIVR01HL079555 · NHLBI · CHILDREN'S RESEARCH INSTITUTE · PI STREISAND, RANDI · 2004 to 2007
$1.8M
Upper Airway Nerve Injury in Apnea: BIP-CHOP-SIRT1 CrosstalkR01HL096037 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI VEASEY, SIGRID C · 2010 to 2013
$1.6M
NHLBI NIH HHS HL079555NHLBI NIH HHS HL096037NHLBI NIH HHS R01 HL079555NHLBI NIH HHS R01 HL079588NHLBI NIH HHS R01 HL096037
6 · The paper itself

Abstract

STUDY

objectivesObstructive sleep apnea (OSA) is associated with cognitive impairment and neuronal injury. Long-term exposure to intermittent hypoxia (LTIH) in rodents, modeling the oxygenation patterns in sleep apnea, results in NADPH oxidase 2 (Nox2) oxidative injury to many neuronal populations. Brainstem motoneurons susceptible to LTIH injury show uncompensated endoplasmic reticulum stress responses with increased (CCAAT/enhancer binding protein homologous protein (CHOP). We hypothesized that CHOP underlies LTIH oxidative injury. In this series of studies, we first determined whether CHOP is upregulated in other brain regions susceptible to LTIH oxidative Nox2 injury and then determined whether CHOP plays an adaptive or injurious role in the LTIH response. To integrate these findings with previous studies examining LTIH neural injury, we examined the role of CHOP in Nox2, hypoxia-inducible factor-1α (HIF-1α) responses, oxidative injury and apoptosis, and neuron loss.

designWithin/between mice subjects.

settingLaboratory setting. PARTICIPANTSSUBJECTS: CHOP null and wild-type adult male mice.

interventionsLTIH or sham LTIH. MEASUREMENTS AND MAIN

resultsRelative to wild-type mice, CHOP-/- mice conferred resistance to oxidative stress (superoxide production/ carbonyl proteins) in brain regions examined: cortex, hippocampus, and motor nuclei. CHOP deletion prevented LTIH upregulation of Nox2 and HIF-1α in the hippocampus, cortex, and brainstem motoneurons and protected mice from neuronal apoptosis and motoneuron loss.

conclusionsEndogenous CHOP is necessary for LTIH-induced HIF-1α, Nox2 upregulation, and oxidative stress; CHOP influences LTIH-induced apoptosis in neurons and loss of neurons. Findings support the concept that minimizing CHOP may provide neuroprotection in OSA.

Indexed as

Analysis of VarianceAnimalsApoptosisBlotting, WesternBrainDisease Models, AnimalHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMice, Inbred C57BLMotor NeuronsNADPH OxidasesOxidative StressReal-Time Polymerase Chain ReactionSleep Apnea SyndromesTranscription Factor CHOPHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitNADPH OxidasesTranscription Factor CHOPGADD153 and gp91phoxHypoxiaPERKreoxygenationunfolded protein response

Identifiers

PMID23564995
PMCPMC3612250
OpenAlexW1982306599

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.