Evidence map›Paper›PMID 39737120›Full record

ArticleCytoJournal2024

Transglutaminase 2 inhibition ameliorates cardiac fibrosis in myocardial infarction by inducing M2 macrophage polarization

Alimujiang Maimaitijiang, Qingyu Huang, Yurong Wu, Shengjia Sun, Qiying Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in CytoJournal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Rewiring the scar: translational advances in cardiac fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    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

5 authors.

Alimujiang MaimaitijiangDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Qingyu HuangDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Yurong WuDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Shengjia SunDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Qiying ChenDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Macrophages perform vital functions in cardiac remodeling after myocardial infarction (MI). Transglutaminase 2 (TG2) participates in fibrosis. Nevertheless, the role of TG2 in MI and mechanisms underlying macrophage polarization are unclear. This study aimed to discover the functions and possible mechanisms of TG2 in MI. Material and Methods: C57BL/6 mice were classified into three groups (six mice per group): Sham, MI, and MI+GK921 groups. GK921 acts as a TG2 inhibitor. Cardiac function, myocardial cell apoptosis, fibrosis, and macrophage phenotype in mouse experiments were detected through echocardiography, terminal deoxynucleotidyl transferase dUTP nick end labeling, Masson staining, immunofluorescence, and flow cytometry, respectively. The Results: In Conclusion: TG2 inhibition facilitated M2 macrophage polarization to provide protection against MI-caused cardiac fibrosis in mice, and these effects may be attained through modulation of the TGF-β1/Smad3 pathway.

Indexed as

Macrophage polarizationMyocardial infarctionTransforming growth factor β1/small mother against decapentaplegic 3 pathwayTransglutaminase 2

Identifiers

PMID39737120
PMCPMC11683372

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.