Evidence map›Paper›PMID 37386574›Full record

ArticleJournal of translational medicine2023

Inhibition of DRP1-dependent mitochondrial fission by Mdivi-1 alleviates atherosclerosis through the modulation of M1 polarization.

Ze-da-Zhong Su, Chun-Qiu Li, Hua-Wei Wang, Min-Ming Zheng, Qing-Wei Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
13.1field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 85 citations in OpenAlex.

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10 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Ze-da-Zhong Su *Department of General Practice, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Chun-Qiu Li *Department of General Practice, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Hua-Wei WangDepartment of General Practice, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Min-Ming ZhengDepartment of Ophthalmology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. 304239@hospital.cqmu.edu.cn.
Qing-Wei ChenDepartment of General Practice, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. chenqwcq@163.com.
Chongqing Medical University · CNDalian Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammation and immune dysfunction with classically activated macrophages(M1) infiltration are important mechanisms in the progression of atherosclerosis (AS). Dynamin-related protein 1 (DRP1)-dependent mitochondrial fission is a novel target for alleviating inflammatory diseases. This study aimed to investigate the effects of DRP1 inhibitor Mdivi-1 on AS.

methodsApoE

resultsIn vivo, Mdivi-1 reduced the plaque areas, M1 polarization, NLRP3 activation and DRP1 phosphorylation at Ser616. In vitro, oxidized low-density lipoprotein (ox-LDL) triggered M1 polarization, NLRP3 activation and abnormal accumulation of mito-ROS. MCC950 and Mito-TEMPO suppressed M1 polarization mediated foam cell formation. Mito-TEMPO significantly inhibited NLRP3 activation. In addition, Mdivi-1 reduced foam cells by inhibiting M1 polarization. The possible mechanisms responsible for the anti-atherosclerotic effects of Mdivi-1 on reducing M1 polarization were associated with suppressing mito-ROS/NLRP3 pathway by inhibiting DRP1 mediated mitochondrial fission. In vitro, similar results were observed by DRP1 knockdown.

conclusionInhibition of DRP1-dependent mitochondrial fission by Mdivi-1 alleviated atherogenesis via suppressing mito-ROS/NLRP3-mediated M1 polarization, indicating DRP1-dependent mitochondrial fission as a potential therapeutic target for AS.

Indexed as

AtherosclerosisIndenesAdenosine TriphosphateAnimalsDynaminsFuransMiceMitochondrial DynamicsNLR Family, Pyrin Domain-Containing 3 ProteinQuinazolinonesReactive Oxygen Species3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneAdenosine TriphosphateDynaminsFuransIndenesNLR Family, Pyrin Domain-Containing 3 ProteinQuinazolinonesReactive Oxygen SpeciesAtherosclerosisDRP1M1 polarizationMdivi-1Mitochondrial fissionNLRP3 inflammasome

Identifiers

PMID37386574
PMCPMC10311781
OpenAlexW4382631630

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.