Evidence map›Paper›PMID 32430880›Full record

ArticleCell stress & chaperones2020

The multiple organs insult and compensation mechanism in mice exposed to hypobaric hypoxia.

Ning Li, Qiuyue Li, Jinrong Bai, Ke Chen, Hailing Yang, Wenxiang Wang, Fangfang Fan, Yi Zhang, Xianli Meng, Tingting Kuang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cell stress & chaperones, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 46 citations in OpenAlex.

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  17. Protective Effect ofOxidative medicine and cellular longevity · 2022
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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

11 authors at 1 institution in 1 country.

Ning LiSchool of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.ORCID 0000-0002-2396-1408
Qiuyue LiSchool of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Jinrong BaiCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Ke ChenCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Hailing YangSchool of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Wenxiang WangCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Fangfang FanSchool of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Yi ZhangSchool of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Xianli MengSchool of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Tingting KuangSchool of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China. kuangtingting@cdutcm.edu.cn.
Gang FanSchool of Ethnic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China. fangang1111@163.com.
Chengdu University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was first and systematically conducted to evaluate the hypoxia response of the brain, heart, lung, liver, and kidney of mice exposed to an animal hypobaric chamber. First, we examined the pathological damage of the above tissues by Hematoxylin & eosin (H&E) staining. Secondly, biochemical assays were used to detect oxidative stress indicators such as superoxide dismutase (SOD), malondialdehyde (MDA), reduced glutathione (GSH), and oxidized glutathione (GSSG). Finally, the hypoxia compensation mechanism of tissues was evaluated by expression levels of hypoxia-inducible factor 1 alpha (HIF-1α), erythropoietin (EPO), and vascular endothelial growth factor (VEGF). During the experiment, the mice lost weight gradually on the first 3 days, and then, the weight loss tended to remain stable, and feed consumption showed the inverse trend. H&E staining results showed that there were sparse and atrophic neurons and dissolved chromatin in the hypoxia group. And hyperemia occurred in the myocardium, lung, liver, and kidney. Meanwhile, hypoxia stimulated the enlargement of myocardial space, the infiltration of inflammatory cells in lung tissue, the swelling of epithelial cells in hepatic lobules and renal tubules, and the separation of basal cells. Moreover, hypoxia markedly inhibited the activity of SOD and GSH and exacerbated the levels of MDA and GSSG in the serum and five organs. In addition, hypoxia induced the expression of HIF-1α, EPO, and VEGF in five organs. These results suggest hypoxia leads to oxidative damage and compensation mechanism of the brain, heart, lung, liver, and kidney in varying degrees of mice.

Indexed as

Oxidative StressAnimalsBrainHypoxiaHypoxia-Inducible Factor 1, alpha SubunitKidneyLiverLungMaleMiceMice, Inbred BALB CSuperoxide DismutaseVascular Endothelial Growth Factor AWeight LossHypoxia-Inducible Factor 1, alpha SubunitSuperoxide DismutaseVascular Endothelial Growth Factor ACompensation mechanismEPOHIF-1αHypoxiaOxidative stressVEGF

Identifiers

PMID32430880
PMCPMC7479670
OpenAlexW3028342092

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.