Coactivator Associated Arginine Methyltransferase 1 Modulates Cartilage Degeneration and Chondrocyte Apoptosis in Osteoarthritis by Regulating ERK1/2 Signaling Pathway.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 40611524.
- Also identified by DOI 10.1111/acel.70122 and PMC identifier 12341778.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
This study investigates the role and mechanism of Coactivator Associated Arginine Methyltransferase 1 (CARM1) in osteoarthritis (OA). OA is a prevalent joint disease characterized by cartilage degradation, subchondral bone remodeling, and inflammation. Our research revealed that CARM1 expression is significantly increased in the cartilage tissues of OA patients and OA model mice. Experimental results showed that inhibiting CARM1 reduces cartilage matrix degradation and chondrocyte apoptosis, while overexpression of CARM1 exacerbates these conditions. Mechanistically, CARM1 regulates OA progression through the phosphorylation of the ERK1/2 signaling pathway. Inhibition of CARM1 suppresses ERK1/2 activation, thereby reducing extracellular matrix degradation and chondrocyte apoptosis. These findings suggest that the CARM1-ERK1/2 axis is crucial in modulating cartilage matrix metabolism and chondrocyte apoptosis in OA, highlighting CARM1 as a potential therapeutic target for OA treatment.
Medical subject headings
- Chondrocytes
- Protein-Arginine N-Methyltransferases
- Osteoarthritis
- Apoptosis
- MAP Kinase Signaling System