SVF
Level D· Preclinical EvidenceAnimal Study

Heterogeneous human muscle fibroadipogenic progenitors include a DLK1 + subpopulation that prevents fatty infiltration after injury.

Garcia SM., Lau J., Diaz A., Lizarraga M., Chi H., Wague A.

Animal Study on Rotator Cuff, published in Sci Transl Med (2026) — summary generated from the PubMed abstract.

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
Sci Transl Med (2026)
Country
United States
Reported sample size
—
PMID
42555756
DOI
10.1126/scitranslmed.aeb7213

Abstract (original English)

Fatty infiltration and fibrosis drive poor outcomes after chronic muscle injury. Here, we characterized fibroadipogenic progenitor cell (FAP) subpopulations from healthy and injured human rotator cuff muscle by single-cell RNA sequencing, full-spectrum flow cytometry, and functional assays and found distinct subpopulations, including a preadipogenic population that expresses delta-like noncanonical notch ligand 1 (DLK1 + ) and a prefibrogenic population that expresses decay-accelerating factor (CD55 + ). We used in vitro and flow cytometry experiments to show that human FAP lineages displayed unique surface marker expression across adipogenic and fibrogenic differentiation. In chronic human rotator cuff injury, expression of DLK1 RNA and DLK1 protein was decreased compared with that in healthy muscle. Overexpression of DLK1 in primary human FAPs suppressed differentiation into adipocytes in vitro, whereas DLK1 knockdown increased adipogenesis. In an immunodeficient murine model of glycerol-induced acute muscle injury, xenotransplantation of DLK1-overexpressing human FAPs into the injured murine muscle resulted in reduced fatty infiltration after 14 days by histological assessment, supporting a functional role for DLK1 in restraining adipogenesis. Together, we defined molecularly distinct, clinically relevant human FAP subpopulations, established DLK1 as a regulator of adipogeni

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 comes from animal or laboratory studies and has not been confirmed in humans.

How we grade evidence
HumansAnimalsCalcium-Binding ProteinsStem CellsAdipogenesisMembrane ProteinsCell DifferentiationFibrosisMiceMale
Face & SkinShoulderRotator Cuff
View on PubMedDOI

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