ArticleNutrients2024
Protective Effects of Vitamin D on Proteoglycans of Human Articular Chondrocytes through TGF-β1 Signaling.
Article in Nutrients, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Engineered Chondrocalcin From Pichia pastoris: A Dual-Functional Biomaterial for Cartilage Regeneration and Rheumatoid Arthritis Modulation.Biotechnology and bioengineering · 2026Article
- Platelet-Derived Components for Skin and Bone Aging and Age-Associated Pathologies: Mechanisms, Bioengineering Strategies, and Clinical Translation.Molecules (Basel, Switzerland) · 2026Review
- Association between gallstones and arthritis in U.S. adults: A cross-sectional NHANES study.Preventive medicine reports · 2026Article
- Vitamin D and bone health: from physiological function to disease association.Nutrition & metabolism · 2025Review
- Association between vitamin D deficiency, inflammatory markers, and knee osteoarthritis: a retrospective study.Journal of orthopaedic surgery and research · 2025Article
- RIP1 inhibition reduces chondrocyte apoptosis through downregulating nuclear factor-kappa B signaling in a mouse osteoarthritis model.Molecular biology reports · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The extracellular matrix of cartilage primarily constitutes of collagen and aggrecan. Cartilage degradation starts with aggrecan loss in osteoarthritis (OA). Vitamin D (VD) plays an essential role in several inflammation-related diseases and can protect the collagen in cartilage during OA. The present study focused on the role of VD in aggrecan turnover of human articular chondrocytes treated with tumor necrosis factor α (TNF-α) and the possible mechanism. Treatment with different doses of VD and different periods of intervention with TNF-α and TGF-β1 receptor (TGFβR1) inhibitor SB525334 were investigated. The viability of human chondrocytes and extracellular secretion of TGF-β1 were measured. The expression of intracellular TGFβR1 and VD receptor was examined. Transcriptional and translational levels of aggrecan and the related metabolic factors were analyzed. The results showed that TNF-α markedly reduced the viability, TGFβR1 expressions and aggrecan levels of human chondrocytes, and increased disintegrin and metalloproteinase with thrombospondin motifs. The alterations were partially inhibited by VD treatment. Furthermore, the effects of VD were blocked by the TGFβR1 inhibitor SB525334 in TNF-α-treated cells. VD may prevent proteoglycan loss due to TNF-α via TGF-β1 signaling in human chondrocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.