Evidence map›Paper›PMID 30286210›Full record

ArticlePloS one2018

Epigallocatechin-3 gallate prevents pressure overload-induced heart failure by up-regulating SERCA2a via histone acetylation modification in mice.

Lifei Liu, Weian Zhao, Jianxia Liu, Yi Gan, Lingjuan Liu, Jie Tian

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  14. Transcriptional factors in calcium mishandling and atrial fibrillation development.Pflugers Archiv : European journal of physiology · 2021
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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 3 institutions in 1 country.

Lifei LiuDepartment of Anesthesiology, Children's Hospital of Chongqing Medical University, Chongqing, PR China.
Weian ZhaoDepartment of Cardiology, Heart Center, Children's Hospital of Chongqing Medical University, Chongqing, PR China.
Jianxia LiuDepartment of Anesthesiology, Children's Hospital of Chongqing Medical University, Chongqing, PR China.
Yi GanMinistry of Education Key Laboratory of Child Development and Disorders, PR China.
Lingjuan LiuKey Laboratory of Pediatrics in Chongqing, Chongqing, PR China.
Jie TianDepartment of Cardiology, Heart Center, Children's Hospital of Chongqing Medical University, Chongqing, PR China.ORCID 0000-0002-9681-1523
Children's Hospital of Chongqing Medical University · CNChina International Science and Technology Cooperation · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure is a common, costly, and potentially fatal condition. The cardiac sarcoplasmic reticulum Ca-ATPase (SERCA2a) plays a critical role in the regulation of cardiac function. Previously, low SERCA2a expression was revealed in mice with heart failure. Epigallocatechin-3-gallate (EGCG) can function as an epigenetic regulator and has been reported to enhance cardiac function. However, the underlying epigenetic regulatory mechanism is still unclear. In this study, we investigated whether EGCG can up-regulate SERCA2a via histone acetylation and play role in preventing heart failure. For this, we generated a mouse model of heart failure by performing a minimally invasive transverse aortic constriction (TAC) operation and used this to test the effects of EGCG. The TAC+EGCG group showed nearly normal cardiac function compared to that in the SHAM group. The expression of SERCA2a was decreased at both the mRNA and protein levels in the TAC group but was enhanced in the TAC+EGCG group. Levels of AcH3 and AcH3K9 were determined to decrease near the promoter region of Atp2a2 (the gene encoding SERCA-2a) in the TAC group, but were elevated in the TAC+EGCG group. Meanwhile, HDAC1 activity and binding near the Atp2a2 promoter were increased in the TAC group but decreased with EGCG addition. Further, binding levels of GATA4 and Mef2c near the Atp2a2 promoter region were reduced in TAC hearts, which might have been caused by histone hypoacetylation; this was reversed by EGCG. Together, upregulation of SERCA2a via the modification of histone acetylation plays a role in EGCG-mediated prevention of pressure overload-induced heart failure, and this might represent a novel pharmacological target for the treatment of heart failure.

Indexed as

AcetylationAnimalsAortic DiseasesCardiovascular AgentsCatechinConstriction, PathologicDisease Models, AnimalHeart FailureHistone Deacetylase 1HistonesMaleMice, Inbred C57BLPromoter Regions, GeneticProtective AgentsRandom AllocationRNA, MessengerAtp2a2 protein, mouseCardiovascular AgentsCatechinepigallocatechin gallateHdac1 protein, mouseHistone Deacetylase 1HistonesProtective AgentsRNA, MessengerSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID30286210
PMCPMC6171916
OpenAlexW2894740271

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.