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

Calcium silicate-stimulated adipose-derived stem cells promote angiogenesis and improve skin wound healing.

Wang M., Zhan H., Wang J., Song H., Sun J., Zhao G.

Animal Study on Chronic Wound, Scar, published in Aging (Albany NY) (2023) — 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
Aging (Albany NY) (2023)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
37263631
PMCID
PMC10292880
DOI
10.18632/aging.204760
Citations
6

Abstract (original English)

Skin wound healing is a complicated process involving proliferation, inflammation, coagulation, and hemostasis, and scar tissue formation of wound repairing. Adipose-derived stem cells (ADSCs) have presented potential therapeutic effects in the non-healing and chronic wound. Calcium silicate (CS) ceramics have been identified as a new type of bioceramics for tissue construction and regeneration. Here, we aimed to explore the impact of CS on the regulation of ADSCs-mediated wound healing. Significantly, CS was able to dose-dependently enhance the proliferation of ADSCs. CS inhibited terminal deoxynucleotidyl transferase dUTP nick end labeling positive cells in the H 2 O 2 -treated ADSCs. Similarly, the Bcl-2 expression was elevated while Bax and cleaved caspase-3 expression were repressed by CS in the cells. CS could induce migration and reduce oxidative stress of ADSCs. Moreover, immunofluorescence analysis and Western blot analysis showed that CS could promote CXCR4 expression in ADSCs. Moreover, CS-stimulated ADSCs enhanced migration and angiogenic capacity of HUVEC. Importantly, CS-stimulated ADSCs improved wound healing in full-thickness skin defect mouse model. Thus, we conclude that CS improves ADSCs-attenuated wound healing in vivo and in vitro . Our finding presents novel insight in the scenario that CS regulates ADSCs and wound healing. CS may be applied as potential m

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
MiceAnimalsAdipose TissueHydrogen PeroxideStem CellsSkinWound HealingCalcium CompoundsSilicates

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