Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

PRMT1 inhibition enhances the cardioprotective effect of adipose-derived mesenchymal stem cells against myocardial infarction through RUNX1.

Du D., Wang T., Sun Y., Zhang Y., Zhang B., Shao J.

Animal Study on Cardiovascular Disease, published in Stem Cell Res Ther (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Stem Cell Res Ther (2025)
Country
England
Reported sample size
—
Source database
PubMed
PMID
40462184
PMCID
PMC12135242
DOI
10.1186/s13287-025-04409-z
Citations
2

Abstract (original English)

Background The poor viability and paracrine function of transplanted mesenchymal stem cells (MSCs) hamper their therapeutic efficacy in ischemic heart injury treatment. Protein arginine methyltransferases (PRMTs) mediate arginine methylation and have important functions in cellular responses. However, the role of PRMTs in MSC-based therapies for ischemic heart injury remains unclear. The aim of this study was to investigate the effect of PRMT1 on MSC function and therapeutic efficacy using a mouse myocardial infarction (MI) model. Methods We isolated, cultured, and identified mouse adipose tissue-derived mesenchymal stromal cells (ADSCs). We used Furamidine, a PRMT1 inhibitor, and adenoviral shPRMT1 to study the effects of PRMT1 inhibition on ADSC proliferation, migration, and viability. We performed RNA sequencing and biochemical experiments to elucidate the molecular mechanisms of PRMT1 in ADSCs. Finally, we infected ADSCs with adenoviral shPRMT1 and administered an intramyocardial injection after MI. Cardiac function was evaluated using echocardiography and pathological staining, and ADSCs survival rates, cardiomyocyte apoptosis, and capillary density were evaluated using immunofluorescence staining. Results We found that PRMT1 was highly expressed in ADSCs and markedly upregulated in response to H 2 O 2 challenge. Inhibition of PRMT1 by Furamidine or adenoviral shPRMT1 prom

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AnimalsProtein-Arginine N-MethyltransferasesMyocardial InfarctionMesenchymal Stem CellsMiceMesenchymal Stem Cell TransplantationAdipose TissueMaleCell ProliferationMice, Inbred C57BL

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