Evidence map›Paper›PMID 25843188›Full record

ArticleAntioxidants & redox signaling2015

Critical Role of Endoplasmic Reticulum Stress in Chronic Intermittent Hypoxia-Induced Deficits in Synaptic Plasticity and Long-Term Memory.

Lin-Hao Xu, Hui Xie, Zhi-Hui Shi, Li-Da Du, Yun-Kwok Wing, Albert M Li, Ya Ke, Wing-Ho Yung

Open access · hybridAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 81 citations in OpenAlex.

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  4. Pharmacological modulation of HIF-1 in the treatment of neuropsychiatric disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2023
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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 2 institutions in 2 countries.

Lin-Hao Xu1 Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong , Shatin, Hong Kong, China .
Hui Xie1 Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong , Shatin, Hong Kong, China .
Zhi-Hui Shi1 Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong , Shatin, Hong Kong, China .
Li-Da Du1 Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong , Shatin, Hong Kong, China .
Yun-Kwok Wing2 Department of Psychiatry, Prince of Wales Hospital , Shatin, Hong Kong, China .
Albert M Li3 Department of Pediatrics, Prince of Wales Hospital , Shatin, Hong Kong, China .
Ya Ke1 Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong , Shatin, Hong Kong, China .
Wing-Ho Yung1 Faculty of Medicine, School of Biomedical Sciences, The Chinese University of Hong Kong , Shatin, Hong Kong, China .
Chinese University of Hong Kong · HKPrince of Wales Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThis study examined the role of endoplasmic reticulum (ER) stress in mediating chronic intermittent hypoxia (IH)-induced neurocognitive deficits. We designed experiments to demonstrate that ER stress is initiated in the hippocampus under chronic IH and determined its role in apoptotic cell death, impaired synaptic structure and plasticity, and memory deficits.

resultsTwo weeks of IH disrupted ER fine structure and upregulated ER stress markers, glucose-regulated protein 78, caspase-12, and C/EBP homologous protein, in the hippocampus, which could be suppressed by ER stress inhibitors, tauroursodeoxycholic acid (TUDCA) and 4-phenylbutyric acid. Meanwhile, ER stress induced apoptosis via decreased Bcl-2, promoted reactive oxygen species production, and increased malondialdehyde formation and protein carbonyl, as well as suppressed mitochondrial function. These effects were largely prevented by ER stress inhibitors. On the other hand, suppression of oxidative stress could reduce ER stress. In addition, the length of the synaptic active zone and number of mature spines were reduced by IH. Long-term recognition memory and spatial memory were also impaired, which was accompanied by reduced long-term potentiation in the Schaffer collateral pathway. These effects were prevented by coadministration of the TUDCA. INNOVATION AND

conclusionThese results show that ER stress plays a critical role in underlying memory deficits in obstructive sleep apnea (OSA)-associated IH. Attenuators of ER stress may serve as novel adjunct therapeutic agents for ameliorating OSA-induced neurocognitive impairment.

Indexed as

Endoplasmic Reticulum StressMemory, Long-TermNeuronal PlasticityAnimalsCaspase 3HippocampusHypoxiaMaleMemoryMice, Inbred C57BLMitochondriaNeuronsPhenylbutyratesProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesSpine4-phenylbutyric acidCaspase 3PhenylbutyratesProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesTaurochenodeoxycholic Acidursodoxicoltaurine

Identifiers

PMID25843188
PMCPMC4580307
OpenAlexW2334695248

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.