Evidence map›Paper›PMID 30031269›Full record

ArticleRedox biology2018

Melatonin improves cardiac function in a mouse model of heart failure with preserved ejection fraction.

Yuan Liu, Li-Na Li, Sen Guo, Xiao-Yan Zhao, Yu-Zhou Liu, Cui Liang, Sheng Tu, Dan Wang, Ling Li, Jian-Zeng Dong and 2 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 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

12 authors at 1 institution in 1 country.

Yuan LiuDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Li-Na LiDepartment of Anaesthesiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Sen GuoDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xiao-Yan ZhaoDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yu-Zhou LiuDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Cui LiangDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Sheng TuDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Dan WangDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Ling LiDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jian-Zeng DongDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Lu GaoDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Electronic address: gaomei1215@163.com.
Hai-Bo YangDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Electronic address: yhb160320@163.com.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melatonin has been shown to inhibit myocardial infarction-induced apoptosis, its function in heart failure with preserved ejection fraction (HFpEF) has not been investigated. This study aimed to investigate whether melatonin attenuates obesity-related HFpEF. Male mice were fed a high-fat diet (HFD) from weaning to 6 months of age to induce HFpEF. The mice were orally administered melatonin (50 mg/kg) by 3 weeks. Diastolic function was significantly improved by melatonin supplementation in mice fed an HFD. Melatonin attenuated obesity-induced myocardial oxidative stress and apoptosis and promoted the secretion of C1q/tumour necrosis factor-related protein 3 (CTRP3) by adipose tissue. And depletion of circulating CTRP3 largely abolished melatonin-mediated cardio-protection. Melatonin-mediated secretion of adipocyte-derived CTRP3 activated NF-E2-related factor 2 (Nrf2), which were largely abrogated by knocking down CTRP3 in adipocytes or Nrf2 in cardiomyocytes. Nrf2 activation was mediated by miR-200a, and a miR-200a antagomir offset the effects of melatonin-conditioned medium on Nrf2 expression. Our results indicate that melatonin can be used to treat and prevent obesity-related HFpEF.

Indexed as

AdipokinesAnimalsAntioxidantsApoptosisDiet, High-FatDisease Models, AnimalHeart FailureMaleMelatoninMiceMice, Inbred C57BLMyocardiumNF-E2-Related Factor 2ObesityOxidative StressStroke VolumeAdipokinesAntioxidantsCORS26 protein, mouseMelatoninNfe2l2 protein, mouseNF-E2-Related Factor 2AdipocyteApoptosisCTRP3HFpEFMelatoninOxidative stress

Identifiers

PMID30031269
PMCPMC6076208
OpenAlexW2852891808

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.