Evidence map›Paper›PMID 29915390›Full record

ArticleScientific reports2018

Gallic acid improves cardiac dysfunction and fibrosis in pressure overload-induced heart failure.

Li Jin, Simei Sun, Yuhee Ryu, Zhe Hao Piao, Bin Liu, Sin Young Choi, Gwi Ran Kim, Hyung-Seok Kim, Hae Jin Kee, Myung Ho Jeong

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Role of gallic acid in sarcopenia in D-galactose-treated mice.Iranian journal of basic medical sciences · 2026
    Article
  3. Review
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  7. Review
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  10. Frontiers in pharmacology · 2025
    Review
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  14. Raspberry polyphenols target molecular pathways of heart failure.The Journal of nutritional biochemistry · 2024
    Article
  15. Article
  16. Review
  17. Review
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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

10 authors at 5 institutions in 2 countries.

Li JinThe Second Affiliated Hospital & Yuying Children's Hospital Wenzhou Medical University, Wenzhou, 325027, China.
Simei SunHeart Research Center of Chonnam National University Hospital, Gwangju, 61469, Republic of Korea.
Yuhee RyuHeart Research Center of Chonnam National University Hospital, Gwangju, 61469, Republic of Korea.
Zhe Hao PiaoThe Second Affiliated Hospital & Yuying Children's Hospital Wenzhou Medical University, Wenzhou, 325027, China.
Bin LiuThe Second Hospital of Jilin University, Changchun, Jilin, 130041, China.
Sin Young ChoiHeart Research Center of Chonnam National University Hospital, Gwangju, 61469, Republic of Korea.
Gwi Ran KimHeart Research Center of Chonnam National University Hospital, Gwangju, 61469, Republic of Korea.
Hyung-Seok KimDepartment of Forensic Medicine, Chonnam National University Medical School, Gwangju, 61469, Republic of Korea.
Hae Jin KeeHeart Research Center of Chonnam National University Hospital, Gwangju, 61469, Republic of Korea. sshjkee@empas.com.
Myung Ho JeongHeart Research Center of Chonnam National University Hospital, Gwangju, 61469, Republic of Korea. myungho@chollian.net.
Chonnam National University Hospital · KRChonnam National University · KRFirst Hospital of Jiaxing · CNSecond Affiliated Hospital of Jilin University · CNSecond Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gallic acid is a trihydroxybenzoic acid found in tea leaves and some plants. Here, we report the effect of gallic acid on cardiac dysfunction and fibrosis in a mouse model of pressure overload-induced heart failure and in primary rat cardiac fibroblasts, and compare the effects of gallic acid with those of drugs used in clinics. Gallic acid reduces cardiac hypertrophy, dysfunction, and fibrosis induced by transverse aortic constriction (TAC) stimuli in vivo and transforming growth factor β1 (TGF-β1) in vitro. It decreases left ventricular end-diastolic and end-systolic diameter, and recovers the reduced fractional shortening in TAC. In addition, it suppresses the expression of atrial natriuretic peptide, brain natriuretic peptide, skeletal α-actin, and β-myosin heavy chain. Administration of gallic acid decreases perivascular fibrosis, as determined by Trichrome II Blue staining, and reduces the expression of collagen type I and connective tissue growth factor. However, administration of losartan, carvedilol, and furosemide does not reduce cardiac dysfunction and fibrosis in TAC. Moreover, treatment with gallic acid inhibits fibrosis-related genes and deposition of collagen type I in TGF-β1-treated cardiac fibroblasts. These results suggest that gallic acid is a therapeutic agent for cardiac dysfunction and fibrosis in chronic heart failure.

Indexed as

PressureAnimalsAortaBiomarkersCardiomegalyConstriction, PathologicFibrosisGallic AcidGene Expression RegulationHeartHeart FailureMaleMiceTransforming Growth Factor beta1BiomarkersGallic AcidTransforming Growth Factor beta1

Identifiers

PMID29915390
PMCPMC6006337
OpenAlexW2807828152

What OpenQuestion holds

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LicenceCC BY
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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.