ArticleThe Journal of arthroplasty2025
The Otto Aufranc Award: DNMT3A-PPARγ Signaling Is a Key Epigenetic Mechanism of Hip Osteoarthritis Disease: A Potential Therapeutic Target.
Article in The Journal of arthroplasty, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Lipid-Driven Immunometabolism in Mesenchymal Stromal Cells: A New Axis for Musculoskeletal Regeneration.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundFemoroacetabular impingement is the leading cause of hip osteoarthritis (OA) and has been linked to 50% of total hip arthroplasty (THA) cases. Still, the mechanism by which the joint progresses to OA remains unknown. Previous studies indicate that peroxisome proliferator-activated receptor gamma (PPARγ) suppression occurred during hip OA progression. We have observed the hypermethylation of the CpG PPARγ promoter area through DNA methyltransferase 3A (DNMT3A), resulting in cartilage catabolism and hip OA. However, its precise mechanism remains unclear. We hypothesized that DNMT3A gain-of-function (GOF) leads to chondrocyte catabolism through PPARγ suppression, and DNMT3A loss-of-function (LOF) rescues the catabolism in OA chondrocytes.
methodsHealthy chondrocytes were isolated from osteochondral allografts, and OA chondrocytes from patients undergoing THA secondary to femoroacetabular impingement disease. Chondrocytes were treated to evaluate the GOF and LOF effects of DNMT3A using lentiviral particles. Interleukin 1 beta (IL1β) was used to mimic the OA phenotype in healthy chondrocytes. Groups included a scramble control, DNMT3A GOF, IL1β+scramble control, IL1β+DNMT3A GOF, and IL1β+DNMT3A LOF for healthy chondrocytes, and scramble control, DNMT3A GOF, and DNMT3A LOF for OA chondrocytes. The DNMT3A, PPARγ, Col2, and MMP13 expression levels were analyzed, with significance set at P < 0.05.
resultsThe IL1β treatment and DNMT3A GOF in healthy chondrocytes significantly increased DNMT3A and MMP13 while decreasing PPARγ and Col2 expression. The DNMT3A LOF in IL1β-treated chondrocytes increased PPARγ and Col2 and decreased MMP13 expression. In OA chondrocytes, DNMT3A GOF increased MMP13 expression while suppressing PPARγ and Col2, whereas DNMT3A LOF resulted in opposite effects, suggesting DNMT3A LOF treatment can alleviate catabolic changes.
conclusionsThe DNMT3A LOF treatment partly reversed chondrocyte degeneration and catabolism, positioning the modulation of DNMT3A as a potential therapeutic intervention in hip OA progression.
Indexed as
Identifiers
What OpenQuestion holds
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.