Evidence map›Paper›PMID 39388091›Full record

ArticleJournal of cardiovascular translational research2025

Drp1 Promotes Macrophage M1 Polarization and Inflammatory Response in Autoimmune Myocarditis by Driving Mitochondrial Fission.

Lin Lin, Jin Wei, Jiahong Xue, Gang Fan, Wenjing Zhu, Yanhe Zhu, Ruiyun Wu

Abstract read
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In one paragraph

Article in Journal of cardiovascular translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Outer membrane vesicles derived from probioticFrontiers in immunology · 2025
    Article
  7. Review
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

7 authors.

Lin LinDepartment of Cardiovascular Medicine, Cardiovascular Hospital of the Second Affiliated Hospital of Xi'an Jiaotong University, Daminggong Campus, No. 5 Jianqiang Road, Xi'an, 710016, Weiyang District, China. lin_linvas@126.com.ORCID 0000-0002-0134-234X
Jin WeiDepartment of Cardiovascular Medicine, Cardiovascular Hospital of the Second Affiliated Hospital of Xi'an Jiaotong University, Daminggong Campus, No. 5 Jianqiang Road, Xi'an, 710016, Weiyang District, China.
Jiahong XueDepartment of Cardiovascular Medicine, Cardiovascular Hospital of the Second Affiliated Hospital of Xi'an Jiaotong University, Daminggong Campus, No. 5 Jianqiang Road, Xi'an, 710016, Weiyang District, China.
Gang FanSecond Department of Cardiology, Xianyang First People's Hospital, Shaanxi University of Chinese Medicine, Xianyang, 712000, China.
Wenjing ZhuDepartment of Cardiovascular Medicine, Cardiovascular Hospital of the Second Affiliated Hospital of Xi'an Jiaotong University, Daminggong Campus, No. 5 Jianqiang Road, Xi'an, 710016, Weiyang District, China.
Yanhe ZhuInstitute of Endiquidiopathies, School of Public Health, Xi'an Jiaotong University, Xi'an, 710061, China.
Ruiyun WuDepartment of Internal Medicine, Xi'an Jiaotong University Health Science Center, Xi'an, 710061, China.

Funding

Shaanxi Provincial Natural Science Foundation Key R&D Program 2024SF-YBXM-005
6 · The paper itself

Abstract

Autoimmune myocarditis (AM) is characterized by an intricate inflammatory response within the myocardium. Dynamin-related protein 1 (Drp1), a pivotal modulator of mitochondrial fission, plays a role in the pathogenesis of various diseases. A myosin-induced experimental autoimmune myocarditis (EAM) mouse model was successfully established. Flow cytometry was employed to detect M1/M2-like macrophages. Mitochondrial fragmentation was assessed using Mito-Tracker Red CMXRos. Drp1 was upregulated and activated in EAM mice. Depletion of Drp1 was observed to mitigate inflammation, macrophage infiltration and M1 polarization within the cardiac tissue of EAM mice. In M1-like macrophages derived from the hearts of EAM mice, Drp1 was found to promote mitochondrial fission and diminish mitochondrial fusion. Furthermore, the depletion of Drp1 reduced the NF-κB-related pro-inflammatory response in EAM-associated M1-like macrophages. Drp1 drives mitochondrial fission in macrophages, driving their M1 polarization and the subsequent inflammatory response. Drp1 may represent an effective target for the prevention and treatment of AM.

Indexed as

Autoimmune DiseasesDynaminsMacrophagesMitochondria, HeartMitochondrial DynamicsMyocarditisMyocardiumAnimalsCells, CulturedDisease Models, AnimalInflammation MediatorsMaleMiceMice, Inbred BALB CNF-kappa BPhenotypeDnm1l protein, mouseDynaminsInflammation MediatorsNF-kappa BAutoimmune myocardioptisDrp1EAM mouse modelM1 polarizationMitochondrial fission

Identifiers

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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.