Evidence map›Paper›PMID 28386372›Full record

ArticleAmerican journal of translational research2017

Thioredoxin-2 protects against oxygen-glucose deprivation/reperfusion injury by inhibiting autophagy and apoptosis in H9c2 cardiomyocytes.

Yan-Yan Li, Yin Xiang, Song Zhang, Yan Wang, Jie Yang, Wei Liu, Feng-Tai Xue

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.8field-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

12 citing papers in PubMed, 32 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

7 authors at 1 institution in 1 country.

Yan-Yan LiDepartment of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University 1665 Kongjiang Road, Shanghai 200092, P. R. China.
Yin XiangDepartment of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University 1665 Kongjiang Road, Shanghai 200092, P. R. China.
Song ZhangDepartment of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University 1665 Kongjiang Road, Shanghai 200092, P. R. China.
Yan WangDepartment of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University 1665 Kongjiang Road, Shanghai 200092, P. R. China.
Jie YangDepartment of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University 1665 Kongjiang Road, Shanghai 200092, P. R. China.
Wei LiuDepartment of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University 1665 Kongjiang Road, Shanghai 200092, P. R. China.
Feng-Tai XueDepartment of Cardiovascular Diseases, Xinhua Hospital, School of Medicine, Shanghai Jiaotong University 1665 Kongjiang Road, Shanghai 200092, P. R. China.
XinHua Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study is to examine the role of thioredoxin-2 (Trx2) in autophagy and apoptosis during myocardial ischemia-reperfusion (I/R) injury in vitro. We employed the oxygen-glucose deprivation and reperfusion (OGD/R) model of H9c2 cells and used lentiviral infection to overexpress Trx2. H9c2 cell viability and injury assays were conducted using a Cell Counting Kit-8 (CCK-8) and alactate dehydrogenase (LDH) kit. The effects of Trx2 on autophagy and apoptosis were measured by transmission electron microscopy (TEM), western blot, and flow cytometry. Our results showed that the expression of Trx2 was significantly decreased at reperfusion 6 h after OGD 12 h treatment. Trx2 overexpression inhibited autophagy in H9c2 cells subjected to OGD/R. As the underlying mechanisms, both Akt kinase/the mammalian target of rapamycin (Akt/mTOR) and AMP-activated protein kinase (AMPK)/mTOR signaling pathways were involved in the regulation of Trx2 during autophagy, which was also mediated by reactive oxygen species (ROS). 3-methyladenine (3-MA), an inhibitor of autophagy, not only suppressed OGD/R-induced autophagy but also decreased apoptosis. As a classical autophagy sensitizer, rapamycin (Rapa) augmented autophagy as well as apoptosis. Additionally, we further demonstrated that Trx2 could alleviate OGD/R-induced apoptosis via mitochondrion-mediated intrinsic apoptotic pathway. In summary, our data indicated that Trx2 protects cardiomyocytes under OGD/R by inhibiting autophagy and apoptosis. Trx2 may be a crucial regulatory protein during I/R-induced cardiomyocyte injury and death.

Indexed as

apoptosisautophagyoxygen-glucose deprivation and reperfusionTrx2

Identifiers

PMID28386372
PMCPMC5376037
OpenAlexW2611232956

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.