Evidence map›Paper›PMID 33613526›Full record

ArticleFrontiers in immunology2020

Exosomes Derived From Hypertrophic Cardiomyocytes Induce Inflammation in Macrophages

Hui Yu, Lei Qin, Yunzhi Peng, Wenhui Bai, Zhanli Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. 80 years of extracellular vesicles: from discovery to clinical translation.Extracellular vesicles and circulating nucleic acids · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. The AGO2-ATOX1 axis exacerbates inflammation in a mouse sepsis model.Central-European journal of immunology · 2026
    Article
  8. Review
  9. Exosomal miRNAs: A New Frontier in Cardiovascular Disease Diagnosis and Treatment.Journal of cardiovascular translational research · 2025
    Review
  10. Review
  11. Review
  12. Review
  13. Small Extracellular Vesicles from Breast Cancer Cells Induce Cardiotoxicity.International journal of molecular sciences · 2025
    Article
  14. Article
  15. Review
  16. miR-31-5p suppresses myocardial hypertrophy by targeting Nfatc2ip.Journal of cellular and molecular medicine · 2024
    Article
  17. Article
  18. Article
  19. Review
  20. Article
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.

Hui YuSchool of Basic Medicine, Baotou Medical College, Baotou, China.
Lei QinGenetic Eugenics Department, Inner Mongolia Maternal and Child Health Care Hospital, Huhhot, China.
Yunzhi PengInner Mongolia Key Laboratory of Disease-Related Biomarkers, Baotou Medical College, Baotou, China.
Wenhui BaiInner Mongolia Key Laboratory of Disease-Related Biomarkers, Baotou Medical College, Baotou, China.
Zhanli WangInner Mongolia Key Laboratory of Disease-Related Biomarkers, Baotou Medical College, Baotou, China.
Baotou Medical College · CNInner Mongolia Maternal and Child Health · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inflammatory immune microenvironment plays an important role in the development of cardiac hypertrophy. Exosomes have emerged as the potent modulators of inflammatory responses. This study aimed to determine how exosomes derived from angiotensin II (Ang II)-induced hypertrophic cardiomyocytes (HCs) interfere with the inflammatory signal pathways in macrophages. Herein, we showed that increased exosome release was observed in HCs when compared to normal cardiomyocytes (NCs). Incubation of the murine macrophage cell line RAW264.7 in the presence of exosomes isolated from the culture media of HCs triggers the secretion of inflammatory cytokines interleukin (IL)-6 and IL-8. Cytokines release induced by HCs-derived exosomes was prevented by down-regulation of Argonaute2 (AGO2), suggesting that the non-coding RNAs were involved in exosome-induced inflammatory responses in RAW 264.7 macrophages. RNA sequencing assays further demonstrated that a total of seven microRNAs were differentially expressed between NCs-derived and HCs-derived exosomes. Importantly, miR-155 played a crucial role in the initiation of inflammation in macrophages. Further analyses demonstrated that HCs-derived exosomes induced the phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38

Indexed as

Angiotensin IIAnimalsAnimals, NewbornCardiomegalyCell CommunicationCellular MicroenvironmentExosomesHumansInflammationInflammation MediatorsInterleukin-6Interleukin-8MacrophagesMiceMicroRNAsMitogen-Activated Protein KinasesAngiotensin IIInflammation MediatorsInterleukin-6interleukin-6, mouseInterleukin-8MicroRNAsMIRN155 microRNA, ratMitogen-Activated Protein Kinasescardiac hypertrophyexosomeinflammationmacrophagemicroRNA

Identifiers

PMID33613526
PMCPMC7886800
OpenAlexW3128409297

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.