Evidence map›Paper›PMID 30311029›Full record

ArticleBiotechnology letters2019

COX6B1 relieves hypoxia/reoxygenation injury of neonatal rat cardiomyocytes by regulating mitochondrial function.

Wei Zhang, Yu Wang, Junzhe Wan, Pengbo Zhang, Fei Pei

Open access · hybridAbstract read
In one paragraph

Article in Biotechnology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 28 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.

Wei ZhangDepartment of Cardiovascular Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 West 5 Road, Xi'an, 710004, Shaanxi Province, China.
Yu WangDepartment of Cardiovascular Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 West 5 Road, Xi'an, 710004, Shaanxi Province, China.
Junzhe WanDepartment of Cardiovascular Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 West 5 Road, Xi'an, 710004, Shaanxi Province, China.
Pengbo ZhangDepartment of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 West 5 Road, Xi'an, 710004, Shaanxi Province, China.
Fei PeiDepartment of Cardiovascular Surgery, The Second Affiliated Hospital of Xi'an Jiaotong University, No.157 West 5 Road, Xi'an, 710004, Shaanxi Province, China. feip_peifx@163.com.
Second Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMitochondrial dysfunction plays a pivotal role in various pathophysiological processes of heart. Cytochrome oxidase subunit 6B1 (COX6B1) is a subunit of cytochrome oxidase.

methodsCardiomyocytes were isolated from neonatal SD rats (within 24 h of birth) by repeating digestion of collagenase and trypsin. COX6B1 over-expression and hypoxia/reoxygenation was conducted on neonatal rat cardiomyocytes. Cell viability, apoptosis rates, mitochondria membrane potential and mitochondrial permeabilization transition pores (mPTPs) were then determined respectively by Cell performing Counting Kit-8 (CCK-8), Annexin-V/PI assay, JC-1 assay, mPTP assay. The expression of cyto C and apoptosis-related factors were detected by RT-Qpcr and Western blot.

resultsHypoxia/reoxygenation increased apoptosis and mPTP levels, and decreased mitochondria membrane potential in I/R and I/R + EV groups. COX6B1 over-expression increased mitochondria cyto C, pro-caspase-3, pro-caspase-9 and bcl-2, while it decreased cytosol cyto C, cleaved-caspase-3, cleaved-caspase-9 and bax compared to I/R + EV group.

conclusionCOX6B1 protected cardiomyocytes from hypoxia/reoxygenation injury by reducing ROS production and cell apoptosis, during which reduction of the release of cytochrome C from mitochondria to cytosol was involved. Our study demonstrated that COX6B1 may be an candidate target gene in preventing hypoxia/reoxygenation injury of cardiomyocytes.

Indexed as

Gene Expression Regulation, EnzymologicAnimalsAnimals, NewbornElectron Transport Complex IVFemaleMitochondria, HeartMuscle CellsMyocardial Reperfusion InjuryRatsRats, Sprague-DawleyElectron Transport Complex IVCardiomyocytesCOX6B1Hypoxia/reoxygenation injuryMitochondria

Identifiers

PMID30311029
PMCPMC6313357
OpenAlexW2896041519

What OpenQuestion holds

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LicenceCC BY
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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.