Evidence map›Paper›PMID 31171760›Full record

ArticleAging2019

E3-ubiquitin ligase TRIM6 aggravates myocardial ischemia/reperfusion injury via promoting STAT1-dependent cardiomyocyte apoptosis.

Guangwei Zeng, Chen Lian, Pei Yang, Mingming Zheng, He Ren, Haiyan Wang

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 14% 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, 26 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

6 authors at 1 institution in 1 country.

Guangwei Zeng *Department of Cardiology, The Second Affiliated Hospital of Air Force Medical University, Shaanxi, China.
Chen Lian *Department of Cardiology, The Second Affiliated Hospital of Air Force Medical University, Shaanxi, China.
Pei Yang *Department of Cardiology, The Second Affiliated Hospital of Air Force Medical University, Shaanxi, China.
Mingming ZhengDepartment of Health Economic Managment, The Second Affiliated Hospital of Air Force Medical University, Shaanxi, China.
He RenDepartment of Cardiology, The Second Affiliated Hospital of Air Force Medical University, Shaanxi, China.
Haiyan WangDepartment of Cardiology, The Second Affiliated Hospital of Air Force Medical University, Shaanxi, China.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiomyocyte apoptosis is a major cause of myocardial ischemia/reperfusion (MI/R) injury, in which the activation of the signal transducer and activator of transcription 1 (STAT1) plays an important role. The E3-ubiquitin ligase TRIM6 has been implicated in regulating STAT1 activity, however, whether it is associated with MI/R injury and the underlying mechanism are not determined. In this study, by investigating a mouse MI/R injury model, we show that TRIM6 expression is induced in mouse heart following MI/R injury. Additionally, TRIM6 depletion reduces and its overexpression increases myocardial infarct size, serum creatine phosphokinase (CPK) level and cardiomyocyte apoptosis in mice subjected to MI/R injury, indicating that TRIM6 functions to aggravate MI/R injury. Mechanistically, TRIM6 promotes IKKε-dependent STAT1 activation, and the inhibition of IKKε or STAT1 with the specific inhibitor, CAY10576 or fludarabine, abolishes TRIM6 effects on cardiomyocyte apoptosis and MI/R injury. Similarly, TRIM6 mutant lacking the ability to ubiquitinate IKKε and induce IKKε/STAT1 activation also fails to promote cardiomyocyte apoptosis and MI/R injury. Thus, these results suggest that TRIM6 aggravates MI/R injury through promoting IKKε/STAT1 activation-dependent cardiomyocyte apoptosis, and that TRIM6 might represent a novel therapeutic target for alleviating MI/R injury.

Indexed as

AnimalsApoptosisCreatine KinaseDisease Models, AnimalI-kappa B KinaseMaleMiceMyocardial IschemiaMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacSTAT1 Transcription FactorTripartite Motif ProteinsUbiquitin-Protein LigasesCreatine KinaseI-kappa B KinaseStat1 protein, mouseSTAT1 Transcription FactorTRIM6 protein, mouseTripartite Motif ProteinsUbiquitin-Protein LigasesapoptosiscardiomyocyteE3-ubiquitin ligase TRIM6myocardial ischemiareperfusion injurySTAT1

Identifiers

PMID31171760
PMCPMC6594808
OpenAlexW2950278245

What OpenQuestion holds

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LicenceCC BY
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.