ArticleDrug design, development and therapy2025
Vitamin D Alleviates Osteoarthritis Progression by Targeting Cartilage and Subchondral Bone via Myd88-TAK1-ERK Axis Suppression.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Capsanthin Attenuates Osteoporosis by Targeting the Urotensin II Receptor Pathway to Inhibit Oxidative Stress and NLRP3 Inflammasome Activation.Calcified tissue international · 2026Article
- Potential value of vitamin D as adjunctive therapy in osteoarticular tuberculosis: a comprehensive review.Infection · 2026Review
- Relation of Serum Vitamin-D Level with Serum Interleukin-6 and Interleukin-10 in Patients with Primary Osteoarthritis of Knee.Journal of orthopaedic case reports · 2025Article
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Authors and funding
10 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Osteoarthritis (OA) causes irreversible joint damage, but current treatments fail to fully address its complex pathology. Emerging evidence suggests subchondral bone metabolic dysfunction may initiate OA. While vitamin D (VitD) is well-established for bone metabolism regulation in osteoporosis, its therapeutic potential in OA remains unclear despite observational studies suggesting protective effects. Our integrated in vivo/in vitro study demonstrates VitD's dual chondroprotective and osteogenic actions in OA. Methods: Sprague-Dawley rats (n=24) were divided into three groups: sham operation (Sham), OA model (OA), and OA+VitD treatment, with 8 rats in each group. Oral cholecalciferol (2.34 μg/kg/day) was administered for 6 weeks post-Monosodium iodoacetate (MIA) induction. The therapeutic potential of vitamin D was evaluated through a series of in vivo experiments. Human chondrocyte C28 cells were pretreated with TNFα (1ng/mL) to model inflammatory injury, followed by 1,25(OH) Results: In OA rats, VitD suppressed femoral cartilage degradation (evidenced by 567.76% increased cartilage area, and 39.13% decreased Osteoarthritis Cartilage Histopathology (OACH) score and enhanced subchondral bone mass (61.81% higher BV/TV). At the molecular level, VitD downregulated the expression of cartilage matrix metalloproteinase 13 (MMP13), with a reduction of 74.72% compared to OA group. Additionally, VitD inhibit inflammatory signaling pathways, particularly through the MyD88-TAK1-ERK axis in chondrocytes, and decrease serum IL-6 level. Mechanistic validation of these findings was demonstrated by protein expression reduction of Myd88 (31.22%), phospho-ERK1/2 (66.11%), AP-1 (61.43%) and NFκB (34.36%) compared to OA group. In vitro, VitD also rescued ethanol-induced C28 cell viability loss while significantly upregulating cartilage anabolic markers. Conclusion: These findings establish VitD as a multimodal OA therapeutic agent targeting both cartilage catabolism and subchondral bone remodeling through Myd88-TAK1-ERK axis.
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