Evidence mapPaperPMID 39845770Full record

ArticleInternational journal of nanomedicine2025

Exosomes Derived from Apelin-Pretreated Mesenchymal Stem Cells Ameliorate Sepsis-Induced Myocardial Dysfunction by Alleviating Cardiomyocyte Pyroptosis via Delivery of miR-34a-5p.

Ting Li, Yuechu Zhao, Zhi Cao, Ying Shen, Jiaqi Chen, Xinran Huang, Zhuang Shao, Yi Zeng, Qi Chen, Xiaofei Yan and 3 more

Abstract read
In one paragraph

Article in International journal of nanomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Involvement of the pyroptosis-HMGB1 axis in systemic diseases.Frontiers in cell and developmental biology · 2026
    Review
  3. Review
  4. Review
  5. 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

13 authors.

Ting Li *School of Medicine, South China University of Technology, Guangzhou, Guangdong, People's Republic of China.ORCID 0009-0005-0946-2871
Yuechu Zhao *Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Zhi Cao *Department of Emergency Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Ying ShenDepartment of Emergency Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Jiaqi ChenDepartment of Emergency Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Xinran HuangDepartment of Emergency Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Zhuang ShaoDepartment of Emergency Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Yi ZengDepartment of Emergency Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Qi ChenDepartment of Emergency Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, People's Republic of China.ORCID 0009-0003-4563-1690
Xiaofei YanGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Xin LiSchool of Medicine, South China University of Technology, Guangzhou, Guangdong, People's Republic of China.
Yuelin ZhangSchool of Medicine, South China University of Technology, Guangzhou, Guangdong, People's Republic of China.
Bei HuSchool of Medicine, South China University of Technology, Guangzhou, Guangdong, People's Republic of China.ORCID 0000-0002-5802-1694

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Exosomes sourced from mesenchymal stem cells (MSC-EXOs) have become a promising therapeutic tool for sepsis-induced myocardial dysfunction (SMD). Our previous study demonstrated that Apelin pretreatment enhanced the therapeutic benefit of MSCs in myocardial infarction by improving their paracrine effects. This study aimed to determine whether EXOs sourced from Apelin-pretreated MSCs (Apelin-MSC-EXOs) would have potent cardioprotective effects against SMD and elucidate the underlying mechanisms. Methods: MSC-EXOs and Apelin-MSC-EXOs were isolated and identified. Mice neonatal cardiomyocytes (NCMs) were treated with MSC-EXOs or Apelin-MSC-EXOs under lipopolysaccharide (LPS) condition in vitro. Cardiomyocyte pyroptosis was determined by TUNEL staining. RNA sequencing was used to identify differentially expressed functional miRNAs between MSC-EXOs and Apelin-MSC-EXOs. MSC-EXOs and Apelin-MSC-EXOs were transplanted into a mouse model of SMD induced by cecal ligation puncture (CLP) via the tail vein. Heart function was evaluated by echocardiography. Results: Compared with MSC-EXOs, Apelin-MSC-EXO transplantation greatly enhanced cardiac function in SMD mice. Both MSC-EXOs and Apelin-MSC-EXOs suppressed cardiomyocyte pyroptosis in vivo and in vitro, with the latter exhibiting superior protective effects. miR-34a-5p effectively mediated Apelin-MSC-EXOs to exert their cardioprotective effects in SMD with high mobility group box-1 (HMGB1) as the potential target. Mechanistically, Apelin-MSC-EXOs delivered miR-34a-5p into injured cardiomyocytes, thereby ameliorating cardiomyocyte pyroptosis via regulation of the HMGB1/AMPK axis. These cardioprotective effects were partially abrogated by downregulation of miR-34a-5p in Apelin-MSC-EXOs. Conclusion: Our study revealed miR-34a-5p as a key component of Apelin-MSC-EXOs that protected against SMD via mediation of the HMGB1/AMPK signaling pathway.

Indexed as

ApelinCardiomyopathiesExosomesMesenchymal Stem CellsMicroRNAsMyocytes, CardiacPyroptosisSepsisAnimalsDisease Models, AnimalHMGB1 ProteinMaleMesenchymal Stem Cell TransplantationMiceMice, Inbred C57BLApelinHMGB1 ProteinMicroRNAsMIRN34a microRNA, mouseapelinExosomesmesenchymal stem cellspyroptosissepsis-induced myocardial dysfunction

Identifiers

PMID39845770
PMCPMC11750946

What Socratic holds

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LicenceCC BY-NC
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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 Socratic graph.