Evidence map›Paper›PMID 29448942›Full record

ArticleBMC cardiovascular disorders2018

Cold exposure induced oxidative stress and apoptosis in the myocardium by inhibiting the Nrf2-Keap1 signaling pathway.

Peifang Cong, Yunen Liu, Nannan Liu, Yubiao Zhang, Changci Tong, Lin Shi, Xuelei Liu, Xiuyun Shi, Ying Liu, Zhou Tong and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-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

23 citing papers in PubMed, 57 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

11 authors at 1 institution in 1 country.

Peifang CongEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Yunen LiuEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Nannan LiuEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Yubiao ZhangEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Changci TongEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Lin ShiEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Xuelei LiuEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Xiuyun ShiEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Ying LiuEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Zhou TongEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China.
Mingxiao HouEmergency Medicine Department of General Hospital of Shenyang Military Command, Laboratory of Rescue Center of Severe Wound and Trauma PLA, No. 83 Road, Shenhe District, Shenyang, l10016, China. houmingxiao188@163.com.ORCID 0000-0001-6865-7007
General Hospital of Shenyang Military Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExposure to cold weather is associated with infaust cardiovascular responses, including myocardial infarction and arrhythmias. However, the exact mechanisms of these adverse changes in the myocardium under cold stress are unknown. This study was designed to investigate the mechanisms of cardiac injury induced by cold stress in mice.

methodsThe mice were randomly divided into three groups, normal control (no handling), 1-week cold stress and 2-week cold stress. We observed physiological changes of the mice and morphological changes of myocardium tissues, and we measured the changes of 3'-nitrotyrosine and 4-hydroxynonenal, the expression levels of superoxide dismutase-1, superoxide dismutase-2, Bax, Bad, Bcl-2, Nuclear factor erythroid-derived 2-like 2 (Nrf2) and Kelch like-ECH-associated protein 1 (Keap1) in myocardium by western blot. Besides, we detected mRNA of superoxide dismutase-1, superoxide dismutase-2, Bax, Bad, Bcl-2, Nrf2 and Keap1 by real-time PCR. One-way analysis of variance, followed by LSD-t test, was used to compare each variable for differences among the groups.

resultsEchocardiography analyses demonstrated left ventricle dysfunction in the groups receiving cold stress. Histological analyses witnessed inflammation, vacuolar and eosinophilic degeneration occurred in left ventricle tissues. Western blotting results showed increased 3'-nitrotyrosine and 4-hydroxynonenal and decreased antioxidant enzymes (superoxide dismutase-1 and superoxide dismutase-2) in the myocardium. Expression of Nrf2 and Keap1 followed a downward trend under cold exposure, as indicated by western blotting and real-time PCR. Expression of anti-apoptotic protein Bcl-2 also showed the same trend. In contrast, expression of pro-apoptotic proteins Bax and Bad followed an upward trend under cold exposure. The results of real-time PCR were consistent with those of western blotting.

conclusionsThese findings were very significant, showing that cold exposure induced cardiac injury by inhibiting the Nrf2-Keap1 signaling pathway.

Indexed as

ApoptosisCold-Shock ResponseCold TemperatureOxidative StressAnimalsApoptosis Regulatory ProteinsDisease Models, AnimalFemaleKelch-Like ECH-Associated Protein 1MaleMiceMyocardiumNF-E2-Related Factor 2Signal TransductionVentricular Dysfunction, LeftVentricular Function, LeftApoptosis Regulatory ProteinsKeap1 protein, mouseKelch-Like ECH-Associated Protein 1Nfe2l2 protein, mouseNF-E2-Related Factor 2ApoptosisCold exposureMiceNrf2Oxidative stress

Identifiers

PMID29448942
PMCPMC5815212
OpenAlexW2796037841

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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.