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Hexokinase 2 Suppression Alleviates the Catabolic Properties in Osteoarthritis via HMGA2 and Contributes to Pulsed
Chuncha Bao1,2, Siyi Zhu1,2, Dejiang Pang3
1Department of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, People's Republic of China.
Abstract:
Abnormalities in glycolytic pathways are prominent factors in the pathogenesis of osteoarthritis (OA). The key glycolytic enzyme Hexokinase 2 (HK2) is highly expressed in chondrocytes in OA; however, its role remains unclear. Pulsed electromagnetic field (PEMF) is commonly used for the treatment of OA. However, the role of PEMF in cartilage damage and the underlying mechanisms are not well understood. Herein, we found that HK2 suppression down-regulated catabolic pathways and alleviated inflammatory responses in OA chondrocytes, whereas HK2 overexpression stimulated inflammation and catabolic levels; moreover, inhibition of HK2 has potential anti-inflammatory and anti-catabolic properties by regulating the expression of HMGA2. PEMF dramatically inhibited the increase in glycolytic activity and catabolic metabolism level in OA and could alleviate the OA phenotype by modulating the HK2/HMGA2 signaling axis. Suppressing HK2 via adeno-associated virus (AAV) in articular cartilage demonstrated that PEMF reduces cartilage damage and OA symptoms through HK2 knockdown. Furthermore, the HK2 inhibitor Lonidamine, in combination with PEMF, more effectively ameliorated cartilage degeneration in OA. Overall, our findings improve understanding of HK2's role in OA and offer new insights for targeting HK2 in treatment. Furthermore, our results provide new clues for the reducing of catabolism and cartilage damage using PEMF.
Insights
Hexokinase 2 (HK2) drives osteoarthritis (OA) by increasing inflammation and cartilage breakdown. Pulsed electromagnetic field (PEMF) therapy reduces OA symptoms by targeting the HK2/HMGA2 pathway, offering new treatment strategies.
Area of Science:
- Biochemistry
- Cell Biology
- Orthopedics
Background:
- Osteoarthritis (OA) pathogenesis involves dysregulated glycolytic pathways.
- Hexokinase 2 (HK2) is upregulated in OA chondrocytes, but its function is unclear.
- Pulsed electromagnetic field (PEMF) therapy is used for OA, yet its mechanisms are poorly understood.
Purpose of the Study:
- To investigate the role of HK2 in OA pathogenesis.
- To elucidate the mechanisms by which PEMF alleviates OA.
- To explore HK2 inhibition as a therapeutic strategy for OA.
Main Methods:
- Studied HK2 expression and function in OA chondrocytes.
- Investigated the effects of HK2 suppression and overexpression.
- Assessed PEMF treatment in OA models.
- Utilized adeno-associated virus (AAV) for HK2 knockdown.
- Examined the combination of PEMF with the HK2 inhibitor Lonidamine.
Main Results:
- HK2 suppression reduced catabolic pathways and inflammation in OA chondrocytes.
- HK2 overexpression promoted inflammation and catabolism.
- PEMF inhibited glycolytic activity and catabolism in OA, modulating the HK2/HMGA2 axis.
- AAV-mediated HK2 knockdown and Lonidamine treatment, alone or with PEMF, ameliorated cartilage damage and OA symptoms.
Conclusions:
- HK2 plays a critical role in OA pathogenesis by regulating inflammation and catabolism.
- PEMF alleviates OA by targeting the HK2/HMGA2 signaling pathway.
- Targeting HK2, potentially combined with PEMF, represents a promising therapeutic approach for OA treatment.
