Evidence map›Paper›PMID 34558649›Full record

ArticleMolecular medicine reports2021

Intermittent hypoxia mimicking obstructive sleep apnea aggravates early brain injury following ICH via neuroinflammation and apoptosis.

Wenjing Fei, Wei Jiao, Xiaoyan Feng, Xufeng Chen, Yuhai Wang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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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 1 country.

Wenjing FeiDepartment of Neurology, 904th Hospital of Joint Logistic Support Force of PLA, Wuxi Clinical College of Anhui Medical University, Wuxi, Jiangsu 214044, P.R. China.
Wei JiaoDepartment of Nursing, 904th Hospital of Joint Logistic Support Force of PLA, Wuxi Clinical College of Anhui Medical University, Wuxi, Jiangsu 214044, P.R. China.
Xiaoyan FengDepartment of Neurosurgery, 904th Hospital of Joint Logistic Support Force of PLA, Wuxi Clinical College of Anhui Medical University, Wuxi, Jiangsu 214044, P.R. China.
Xufeng ChenDepartment of Gastroenterology, 904th Hospital of Joint Logistic Support Force of PLA, Wuxi Clinical College of Anhui Medical University, Wuxi, Jiangsu 214044, P.R. China.
Yuhai WangDepartment of Neurology, 904th Hospital of Joint Logistic Support Force of PLA, Wuxi Clinical College of Anhui Medical University, Wuxi, Jiangsu 214044, P.R. China.
Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spontaneous intracerebral hemorrhage (ICH) is a subtype of stroke associated with high mortality and morbidity due to the lack of effective therapy. Obstructive sleep apnea (OSA) has been reported to aggravate early brain injury (EBI) and worsen the overall outcome of patients with ICH. However, the precise role of OSA‑mediated neuroinflammation and apoptosis following ICH has not been confirmed. The present study aimed to investigate the neuronal damage induced by OSA and the potential molecular mechanisms by which ICH‑induced EBI regulates neural apoptosis in a C57BL/6 mouse ICH model. Mortality, neurological score, brain water content and neuronal death were evaluated by Evans blue extravasation, TUNEL staining, ELISA, analysis of reactive oxygen species/lipid peroxidation and western blotting. The results showed that OSA induction decreased survival rate, neurological score and neuron survival and upregulated the protein expression levels of Caspase‑3, Bax, cytokines IL‑1β, IL‑6 and TNF‑α and NF‑κB, which indicated that OSA‑mediated induction of apoptosis and neuroinflammation aggravated neuronal death following ICH. The molecular mechanism was partly dependent on the activating transcription factor/CHOP pathway. Taken together, the results demonstrated that OSA worsens neurological outcomes in mice and increases neuronal death by enhancing neural apoptosis and neuroinflammation.

Indexed as

ApoptosisActivating Transcription Factor 4AnimalsApoptosis Regulatory ProteinsBiomarkersBlood-Brain BarrierBrainCytokinesDisease Models, AnimalDisease SusceptibilityHypoxiaImmunohistochemistryMaleMiceNeuroinflammatory DiseasesNeuronsActivating Transcription Factor 4Apoptosis Regulatory ProteinsAtf4 protein, mouseBiomarkersCytokinesReactive Oxygen SpeciesTranscription Factor CHOPapoptosisearly brain injuryintracerebral hemorrhageneuroinflammationobstructive sleep apnea

Identifiers

PMID34558649
PMCPMC8485128
OpenAlexW3200288661

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.