Evidence map›Paper›PMID 34336116›Full record

ArticleOxidative medicine and cellular longevity2021

Melatonin Attenuates Diabetic Myocardial Microvascular Injury through Activating the AMPK/SIRT1 Signaling Pathway.

Bin Wang, Jinyu Li, Mi Bao, Runji Chen, Haiyan Li, Binger Lu, Meixin Chen, Danmei Huang, Yanmei Zhang, Fenfei Gao and 1 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Bin WangDepartment of Pharmacology, Shantou University Medical College, Shantou 515041, China.
Jinyu LiDrug Clinical Trial Institution, The Second Affiliated Hospital, Shantou University Medical College, Shantou 515041, China.
Mi BaoDepartment of Pharmacology, Shantou University Medical College, Shantou 515041, China.
Runji ChenDepartment of Pharmacology, Shantou University Medical College, Shantou 515041, China.
Haiyan LiDepartment of Pharmacology, Shantou University Medical College, Shantou 515041, China.
Binger LuDepartment of Pharmacy, The First Affiliated Hospital, Shantou University Medical College, Shantou 515041, China.
Meixin ChenDepartment of Pharmacology, Shantou University Medical College, Shantou 515041, China.
Danmei HuangDepartment of Pharmacology, Shantou University Medical College, Shantou 515041, China.
Yanmei ZhangDepartment of Pharmacology, Shantou University Medical College, Shantou 515041, China.ORCID https://orcid.org/0000-0002-1179-6142
Fenfei GaoDepartment of Pharmacology, Shantou University Medical College, Shantou 515041, China.ORCID https://orcid.org/0000-0003-4144-8891
Ganggang ShiDepartment of Pharmacology, Shantou University Medical College, Shantou 515041, China.ORCID https://orcid.org/0000-0002-6856-1192
Shantou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac microvascular endothelial cell (CMEC) dysfunction is considered as a major contributor to the cardiovascular complications in diabetes mellitus, with oxidative stress caused by hyperglycemia playing a critical role in the progression of CMEC dysfunction. Melatonin is a kind of hormone well known for its antioxidant properties, which has potential protective effects against diabetes mellitus and its complications. However, the role of melatonin on CMEC dysfunction caused by hyperglycemia and its molecular mechanisms underlying these effects has not been clarified. Herein, we investigate the protective effects of melatonin on high glucose- (HG-) evoked oxidative stress and apoptosis in CMECs and underlying mechanisms. Our results revealed that melatonin ameliorated the injury caused by HG in primary cultured rat CMECs. Injury can be accompanied by reduced reactive oxygen species (ROS) and malondialdehyde (MDA) production, and enhanced superoxide dismutase (SOD) activity. Meanwhile, melatonin treatment significantly inhibited HG-induced CMEC apoptosis. Moreover, melatonin increased the activity of the AMPK/SIRT1 signaling axis in CMECs under HG condition, whereas administration of the AMPK inhibitor compound C or SIRT1 silencing partially abrogated the beneficial effects of melatonin. In streptozotocin- (STZ-) evoked diabetic mice, melatonin notably ameliorated cardiac dysfunction and activated the AMPK/SIRT1 signaling. In conclusion, our findings revealed that melatonin attenuates HG-induced CMEC oxidant stress, apoptosis injury, and STZ-induced cardiac dysfunction through regulating the AMPK/SIRT1 signaling pathway.

Indexed as

AMP-Activated Protein KinasesAnimalsAntioxidantsCardiomyopathiesDisease Models, AnimalHumansMaleMelatoninMiceOxidative StressSignal TransductionSirtuin 1AMP-Activated Protein KinasesAntioxidantsMelatoninSirtuin 1

Identifiers

PMID34336116
PMCPMC8292078
OpenAlexW3169693240

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.