Evidence map›Paper›PMID 38092988›Full record

ArticleJournal of cardiovascular translational research2024

CAV1 Protein Encapsulated in Mouse BMSC-Derived Extracellular Vesicles Alleviates Myocardial Fibrosis Following Myocardial Infarction by Blocking the TGF-β1/SMAD2/c-JUN Axis.

Yijin Wu, Wenying Peng, Siyao Chen, Xiaodong Zeng, Jiade Zhu, Ping Zhu

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of cardiovascular translational research, 2024. 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
0.9field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Signaling Pathways and Therapeutic Approaches in Post-Myocardial Infarction Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2025
    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

6 authors at 1 institution in 1 country.

Yijin WuDepartment of Cardiovascular Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, No.106 Zhongshan Er Road, Yuexiu District, Guangzhou, 510100, China.
Wenying PengDepartment of Intensive Care Unit of Cardiovascular Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510100, China.
Siyao ChenDepartment of Intensive Care Unit of Cardiovascular Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510100, China.
Xiaodong ZengDepartment of Intensive Care Unit of Cardiovascular Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, 510100, China.
Jiade ZhuDepartment of Cardiovascular Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, No.106 Zhongshan Er Road, Yuexiu District, Guangzhou, 510100, China.
Ping ZhuDepartment of Cardiovascular Surgery, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, No.106 Zhongshan Er Road, Yuexiu District, Guangzhou, 510100, China. zhuping@gdph.org.cn.ORCID 0009-0004-9184-0677
Guangdong Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular vesicles (EVs) derived from mouse bone marrow mesenchymal stem cells (mBMSCs) convey the CAV1 protein, influencing the TGF-β1/SMAD2/c-JUN pathway and thus the molecular mechanisms underlying myocardial fibrosis (MF) post-myocardial infarction (MI). Through various experimental methods, including transmission electron microscopy, Nanosight analysis, Western blot, ELISA, and qRT-PCR, we isolated, purified, and identified EVs originating from mBMSCs. Bioinformatics and experimental findings show a reduced expression of CAV1 in myocardial fibrosis tissue. Furthermore, our findings suggest that mBMSC-EVs can deliver CAV1 to cardiac fibroblasts (CFs) and that silencing CAV1 in mBMSC-EVs promotes CF fibrosis. In vivo studies further corroborated these findings. In conclusion, mBMSC-EVs mitigate myocardial fibrosis in MI mice by delivering the CAV1 protein, inhibiting the TGF-β1/SMAD2/c-JUN pathway.

Indexed as

Caveolin 1Disease Models, AnimalExtracellular VesiclesFibrosisMesenchymal Stem CellsMice, Inbred C57BLMyocardial InfarctionMyocardiumProto-Oncogene Proteins c-junSignal TransductionSmad2 ProteinTransforming Growth Factor beta1AnimalsCells, CulturedFibroblastsJNK Mitogen-Activated Protein KinasesCav1 protein, mouseCaveolin 1JNK Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-junSmad2 ProteinSmad2 protein, mouseTgfb1 protein, mouseTransforming Growth Factor beta1Bone marrow–derived mesenchymal stem cellsCAV1Extracellular vesiclesMyocardial infarction

Identifiers

PMID38092988
OpenAlexW4389669507

What OpenQuestion holds

Textmetadata
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.