Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Hypoxic ADSC-derived exosomes enhance wound healing in diabetic mice via delivery of circ-Snhg11 and induction of M2-like macrophage polarization.

Shi R., Jin Y., Zhao S., Yuan H., Shi J., Zhao H.

Animal Study on Chronic Wound, published in Biomed Pharmacother (2022) — 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
Read the A–D evidence level guide

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
Biomed Pharmacother (2022)
Country
France
Reported sample size
—
Source database
PubMed
PMID
36076572
DOI
10.1016/j.biopha.2022.113463
Citations
109

Abstract (original English)

Diabetes mellitus is a major cause of blindness and chronic ulcers in the working age population worldwide. Former research have found that differentially expressed circular RNAs (circRNAs) are associated with hyperglycemia (HG)-induced endothelial cell damage. And adipose-derived stem cells (ADSCs)-exosome transplant have more therapeutic effect to enhance wound healing in diabetic mice by delivery circRNA. The current investigation employed high-throughput sequencing to identify circRNAs that are abnormally expressed in endothelial progenitor cells (EPCs) under HG conditions. The regulatory mechanism and predicted targets of one differentially expressed circRNA, circ-Snhg11, were investigated utilizing bioinformatics analyses, luciferase reporter assays, angiogenic differentiation assays, flow cytometric apoptosis analysis, and RT-qPCR. The result show that circ-Snhg11 expression decreased in EPCs under HG conditions and that overexpression of circ-Snhg11 suppressed HG-induced endothelial cell damage and M1-like macrophage polarization. miR-144-3p and HIF-1α were identified as downstream targets of circ-Snhg11, which was further verified by luciferase reporter analysis. miR-144-3p overexpression or HIF-1α inhibition reversed circ-Snhg11 protective effect on HG-induced endothelial cell dysfunction, as evidenced by increased apoptosis, abnormal vascular differentiation, and sec

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
AnimalsCell ProliferationDiabetes Mellitus, ExperimentalExosomesHypoxiaMacrophagesMesenchymal Stem CellsMiceMicroRNAsRNA, Circular

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