Level C· Early human research exploring benefitsProspective StudyPubMed

Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis.

Chen J., Li K., Shao J., Mei S., Lai Z., Zhao H.

Prospective Study on Stroke Research, published in Nat Commun (2026) — summary generated from the PubMed abstract.

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Level C· Early human research exploring benefitsEvidence level of this study

Early human evidence such as case series or small samples is exploring possible benefits.

  • 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
Prospective Study
Journal
Nat Commun (2026)
Country
England
Reported sample size
—
Source database
PubMed
PMID
42135279
DOI
10.1038/s41467-026-72962-z

Abstract (original English)

Atherosclerotic carotid stenosis is a major cause of stroke, yet the mechanisms driving plaque instability remain incompletely understood. Perivascular adipose tissue (PVAT), the fat surrounding blood vessels, has been implicated in advanced atherosclerosis progression, but its cellular contributions are largely unknown. Here we show that PVAT contains two distinct adipose-derived stem cell (ADSC, multipotent progenitor cells within fat tissue) subsets. By analyzing 169 clinical samples using single-cell RNA sequencing and flow cytometry and pathological staining, we identify CD55⁺ADSCs as elevated in patients with symptomatic carotid stenosis or prior stroke. These cells migrate into plaques, differentiate into endothelial cells and promote pathological angiogenesis and vascular remodeling through FGF2 secretion thereby destabilising plaques. A second population, CXCL14 + ADSCs exacerbate inflammation by recruiting immune cells via the CXCL12-CXCR4 axis. Our findings identify perivascular CD55 + ADSCs as a therapeutic target for atherosclerosis management.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

How we grade evidence
HumansAdipose TissueAtherosclerosisAnimalsReceptors, CXCR4Vascular RemodelingChemokine CXCL12Stem CellsMiceEndothelial Cells

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