Evidence map›Paper›PMID 30890937›Full record

ArticleFrontiers in pharmacology2019

Trimetazidine Attenuates Exhaustive Exercise-Induced Myocardial Injury in Rats via Regulation of the Nrf2/NF-κB Signaling Pathway.

Hongming Zhang, Moyan Liu, Yuyan Zhang, Xiaoyan Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  14. Protein fromFood science and biotechnology · 2022
    Article
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  16. Trimetazidine and COVID-19-induced acute cardiac injury: a missed key.International journal of clinical pharmacy · 2022
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  18. Trimetazidine affects pyroptosis by targeting GSDMD in myocardial ischemia/reperfusion injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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

4 authors at 2 institutions in 1 country.

Hongming ZhangDepartment of Cardiology, The General Hospital of Jinan Military Area Command, Jinan, China.
Moyan LiuDepartment of Cardiology, The General Hospital of Jinan Military Area Command, Jinan, China.
Yuyan ZhangDepartment of Cardiology, The Affiliated Hospital of Guilin Medical University, Guilin, China.
Xiaoyan LiDepartment of Cardiology, The General Hospital of Jinan Military Area Command, Jinan, China.
General Hospital of Jinan Military Command · CNGuilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exhausted exercise has been reported to cause the damage of myocardial structure and function in terms of cardiomyocyte apoptosis, oxidative stress, and energy metabolism disturbance. Trimetazidine (TMZ), as an anti-ischemic agent, has been approved to be effective in promoting myocardial energy metabolism, anti-inflammatory, and anti-oxidation. However, few studies examined the effects of TMZ on myocardial injury induced by exhausted exercise. To investigate whether TMZ could ameliorate the exhaustive exercise-induced myocardial injury and explore the underlying mechanisms, here the rat model of exhaustive exercise was induced by prolonged swimming exercise and TMZ was administrated to rats before exhaustive exercise. According to the results, we demonstrated that exhaustive exercise led to cardiomyocyte damage in rats as evidenced by elevations in cTnI and NT-proBNP levels, and decrease in CX43 expression, which was attenuated by TMZ treatment. Moreover, the administration of TMZ was found to restrain exhaustive exercise-induced oxidative stress damage by increasing GSH level, SOD and GSH-Px activities, and decreasing MDA level. Additionally, TMZ ameliorated myocardial injury by inhibiting apoptosis via reducing Bax/Bcl-2 ratio and down-regulating cleaved caspase-3, cleaved PARP, and cytochrome c levels in the myocardium of rats. Furthermore, we found that TMZ suppressed oxidative stress and cardiomyocyte apoptosis via activation of Nrf2/HO-1 and inactivation of NF-κB signaling pathways. Therefore, our study suggested that TMZ provided cardioprotection in rats after exhaustive exercise, indicating TMZ might served as a potential therapeutic drug for exhaustive exercise-induced myocardial injury.

Indexed as

apoptosiscardioprotectionexhaustive exercisemyocardial injuryoxidative stresstrimetazidine

Identifiers

PMID30890937
PMCPMC6411712
OpenAlexW2919756826

What OpenQuestion holds

Textmetadata
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.