Femoroacetabular 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 (PPAR ) suppression occurred during hip OA progression. We have observed the hypermethylation of the CpG PPAR 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 PPAR suppression, and DNMT3A loss-of-function (LOF) rescues the catabolism in OA chondrocytes.
The DNMT3A LOF treatment partly reversed chondrocyte degeneration and catabolism, positioning the modulation of DNMT3A as a potential therapeutic intervention in hip OA progression.
Copyright remains with the authors and publisher.
Femoroacetabular 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 (PPAR ) suppression occurred during hip OA progression. We have observed the hypermethylation of the CpG PPAR 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 PPAR suppression, and DNMT3A loss-of-function (LOF) rescues the catabolism in OA chondrocytes.
The DNMT3A LOF treatment partly reversed chondrocyte degeneration and catabolism, positioning the modulation of DNMT3A as a potential therapeutic intervention in hip OA progression.
Copyright remains with the authors and publisher.