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

Extracellular vesicles secreted by adipose-derived stem cells alleviate dedifferentiation and senescence in monolayer-expanded chondrocytes by suppressing interleukin-1β-induced MAPK signaling.

Wu SC., Chang LH., Wu CW., Chen CH., Chang JK., Ho ML.

Animal Study on Cartilage Damage, published in Cell Transplant (2026) — 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
Cell Transplant (2026)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
42033151
PMCID
PMC13129361
DOI
10.1177/09636897261440426

Abstract (original English)

Autologous chondrocyte implantation (ACI) has long been regarded as the gold-standard chondrocyte-based therapy for articular cartilage repair. The main challenge in ACI is that chondrocytes lose their chondrogenic phenotype after monolayer expansion in vitro . The monolayer-expanded chondrocytes show dedifferentiation and senescence, hindering their ability to synthesize hyaline cartilage. Currently, there is no effective method to alleviate dedifferentiation and senescence in these monolayer-expanded chondrocytes. Adipose-derived stem cells (ADSCs) have been increasingly explored as a viable alternative cell source to chondrocytes for articular cartilage tissue engineering. Besides inducing chondrogenesis of ADSCs into chondrocyte, recent research emphasizes the positive impact of ADSC-secreted extracellular vesicles (ADSC-EVs). We demonstrate that ADSC-EVs alleviate dedifferentiation and senescence in monolayer-expanded chondrocytes, enhancing their capacity to produce hyaline cartilage. The ADSC-EVs treatment redifferentiated the monolayer-expanded chondrocytes by upregulating collagen type II (Col-II), sulfated glycosaminoglycan (sGAG), and SOX-9 expression and decreasing collagen type I (Col-I) levels. The redifferentiated chondrocytes also showed enhanced cell proliferation and reduced levels of P16 and senescence-associated β-galactosidase (SA-β-gal). Moreover, ADSC-EV

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
ChondrocytesExtracellular VesiclesCellular SenescenceInterleukin-1betaAnimalsStem CellsCell DedifferentiationMAP Kinase Signaling SystemAdipose TissueCells, Cultured

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