ShK-modified UCMSCs Inhibit M1-Like Macrophage Polarization and Alleviate Osteoarthritis Progression via PI3K/Akt Axis

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

Abstract (original English)

The potassium channel Kv1.3 plays an important role in regulating immune cell functions in many inflammatory diseases whereas rarely in osteoarthritis (OA). Here, it is demonstrated that the Kv1.3 of macrophages is upregulated in response to LPS stimulation, as well as in human OA synovium samples than non-OA. Administration of Stichodactyla toxin (ShK), a Kv1.3 blocker, significantly inhibited cartilage degeneration and synovial inflammation in animal models of OA in vivo by inhibiting M1 macrophage polarization and reducing the production of inflammatory factors. In this study, a transgenically engineered human umbilical cord mesenchymal stem cell (UCMSC) delivery system is developed that secreted a peptide ShK, a Kv1.3 potassium blocker, into the knee articular cavity. Collectively, the results identified Kv1.3 as a potential therapeutic target for OA and demonstrated the efficacy of using ShK transgenic engineered UCMSCs as a delivery for the peptide in OA treatment.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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