Evidence map›Paper›PMID 35818358›Full record

ArticlePeerJ2022

Ferroptotic cardiomyocyte-derived exosomes promote cardiac macrophage M1 polarization during myocardial infarction.

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

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Intercellular transfer of LncRNABiochemistry and biophysics reports · 2026
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  17. Article
  18. Mechanism of Ferroptosis and Its Role in Disease Development.International journal of biological sciences · 2025
    Review
  19. Article
  20. 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 at 2 institutions in 1 country.

Shengjia SunDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Yurong WuNursing Department, Huashan Hospital, Fudan University, Shanghai, China.
Alimujiang MaimaitijiangDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Qingyu HuangDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Qiying ChenDepartment of Cardiology, Huashan Hospital, Fudan University, Shanghai, China.
Huashan Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is a mode of cell death that occurs in myocardial infarction (MI). Signals emanating from apoptotic cells are able to induce macrophage polarization through exosome-loading cargos, which plays a vital role in the process of disease. However, whether ferroptotic cardiomyocytes derived exosome (MI-Exo) during MI act on macrophage polarization and its mechanism remain unclear. In this study, a MI mouse model was established, and cardiac function evaluation and pathological staining were performed. The effect of MI-Exo on polarization of RAW264.7 cells was assessed by the expression of IL-10 and NOS2. Ferroptosis inhibitor of ferrostatin-1 was used to verify whether MI-Exo function was dependents on ferroptosis. Cardiac function and myocardial histomorphology were markedly impaired and massive immune cell infiltration in MI mice, compared with the sham group. The significantly increased MDA content and Fe

Indexed as

ExosomesMyocardial InfarctionAnimalsCyclohexylaminesInterleukin-10MacrophagesMiceMyocytes, CardiacPhenylenediaminesCyclohexylaminesferrostatin-1Interleukin-10PhenylenediaminesCardiomyocytes derived exosomeFerroptosisMacrophage M1 polarizationMyocardial infarctionWnt/β-cantenin pathway

Identifiers

PMID35818358
PMCPMC9270880
OpenAlexW4283831334

What OpenQuestion holds

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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.