Evidence map›Paper›PMID 37430319›Full record

ArticleJournal of cardiothoracic surgery2023

Dexmedetomidine ameliorates diabetic cardiomyopathy by inhibiting ferroptosis through the Nrf2/GPX4 pathway.

Fan Li, Zhenfei Hu, Yidan Huang, Haiting Zhan

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

Article in Journal of cardiothoracic surgery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.4field-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

27 citing papers in PubMed, 35 citations in OpenAlex.

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  14. Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy.Apoptosis : an international journal on programmed cell death · 2025
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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.

Fan LiDepartment of Anesthesiology, First Afiliated Hospital of Xinjiang Medical University, Xinjiang Perioperative Organ Protection Laboratory (XJDX1411), No.1 Liyushan Road, Urumqi, Xinjiang, 830054, China.
Zhenfei HuDepartment of Anesthesiology, First Afiliated Hospital of Xinjiang Medical University, Xinjiang Perioperative Organ Protection Laboratory (XJDX1411), No.1 Liyushan Road, Urumqi, Xinjiang, 830054, China.
Yidan HuangDepartment of Anesthesiology, First Afiliated Hospital of Xinjiang Medical University, Xinjiang Perioperative Organ Protection Laboratory (XJDX1411), No.1 Liyushan Road, Urumqi, Xinjiang, 830054, China.
Haiting ZhanDepartment of Anesthesiology, First Afiliated Hospital of Xinjiang Medical University, Xinjiang Perioperative Organ Protection Laboratory (XJDX1411), No.1 Liyushan Road, Urumqi, Xinjiang, 830054, China. zhanhaiting1@163.com.
Xinjiang Medical University · CNSixth Affiliated Hospital of Xinjiang Medical University · CN

Funding

Natural Science Foundation Project of Xinjiang Uygur Autonomous Region. No. (2019D01C293)
6 · The paper itself

Abstract

objectiveDexmedetomidine (DEX) has been shown to have anti-apoptotic effects in diabetes mellitus, but its role in mitigating diabetic cardiomyopathy (DCM) through ferroptosis regulation is unclear.

methodsAn in vitro DCM model was established using H9C2 cells induced with high glucose (HG) and treated with DEX at varying doses and a nuclear factor erythroid 2-realated factor 2 (Nrf2) specific inhibitor ML385. Cell viability was evaluated using the MTT method after treatment with DEX or mannitol (MAN), and the dosage of DEX used in subsequent experimentation was determined. The effects of HG-induced high osmotic pressure were assessed using MAN as a control. Cell apoptosis was evaluated using flow cytometry. Protein levels of Bcl2, Bax, nuclear Nrf2, and glutathione peroxidase 4 (GPX4) were measured using Western blot. Superoxide dismutase (SOD) activity, malondialdehyde (MDA) levels, Fe

resultsTreatment with DEX or MAN had no effect on H9C2 cell viability. HG induction reduced H9C2 cell viability, increased cell apoptosis, upregulated levels of Bax, Fe

conclusionOur findings demonstrate that DEX attenuates HG-induced cardiomyocyte injury by inhibiting ferroptosis through the Nrf2/GPX4 pathway, providing potential therapeutic targets for DCM treatment.

Indexed as

DexmedetomidineDiabetes MellitusDiabetic CardiomyopathiesFerroptosisbcl-2-Associated X ProteinHumansMannitolNF-E2-Related Factor 2Reactive Oxygen SpeciesSuperoxide Dismutasebcl-2-Associated X ProteinDexmedetomidineMannitolNF-E2-Related Factor 2Reactive Oxygen SpeciesSuperoxide DismutaseDexmedetomidineDiabetic cardiomyopathyFerroptosisH9C2 cellsNrf2/GPX4 pathwayOxidative stress

Identifiers

PMID37430319
PMCPMC10334540
OpenAlexW4383822583

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.