SVF
Level D· Preclinical EvidenceAnimal Study

NMN-primed exosomes derived from infrapatellar fat pad mesenchymal stem cells exert synergistic anti-inflammatory and cartilage-protective effects via MERTK pathway activation in knee osteoarthritis.

Chen KT., Huang CC., Yadav VK., Pikatan NW., Fong IH., Kuo KT.

Animal Study on Knee Osteoarthritis, Osteoarthritis, Cartilage Damage, Chronic Inflammation, published in Int J Pharm (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
Int J Pharm (2026)
Country
Netherlands
Reported sample size
—
PMID
41213482
DOI
10.1016/j.ijpharm.2025.126367

Abstract (original English)

Osteoarthritis (OA) is a chronic degenerative joint disease lacking effective disease-modifying therapies. This study evaluated the therapeutic potential of nicotinamide mononucleotide (NMN)-primed exosomes derived from infrapatellar fat pad mesenchymal stem cells (IPFP-MSCs), termed Exo NMN(+) , under the hypothesis that NMN priming enhances their anti-inflammatory, antioxidant, and chondroprotective efficacy through MERTK-dependent signaling. Exo NMN(+) were isolated and characterized by nanoparticle tracking analysis and Western blotting, showing enrichment of exosomal markers (CD9, CD63, ALIX) without size alteration, indicating enhanced cargo loading. In IL-1β-stimulated human chondrocytes, Exo NMN(+) improved viability, migration, and proliferation (increased Ki-67 and EdU expression), suppressed catabolic factors (MMP2, MMP9, VEGF), and upregulated anabolic markers (COL2A1, MERTK). Transcriptomic profiling identified 428 uniquely regulated genes, primarily involved in PI3K-AKT and small-GTPase signaling. Intersection analysis with single-cell OA datasets revealed five shared differentially expressed genes forming the basis of the GAS6-MERTK-PI3K/AKT axis. Exo NMN(+) also reduced intracellular reactive oxygen species (by 51 %) and apoptosis (by 60 %), effects abrogated upon MERTK knockdown, confirming pathway specificity. In a papain-induced OA mouse model, intra-articula

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
Mesenchymal Stem CellsExosomesAnimalsHumansOsteoarthritis, KneeAdipose TissueSignal Transductionc-Mer Tyrosine KinaseChondrocytesMale
KneeSystemic / IVKnee OsteoarthritisOsteoarthritisCartilage DamageChronic Inflammation
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