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Abstract
Osteoarthritis (OA) involves progressive cartilage failure influenced by multiple interconnected molecular mechanisms.
- Chondrocytes transition from a state that builds cartilage to one that breaks it down, indicated by increased activity of matrix metalloproteinases.
- Key signaling pathways, such as NF-κB and MAPK, become disrupted, contributing to cartilage matrix degradation.
- Declining autophagy reduces cellular quality control, while the accumulation of senescent cells releases inflammatory substances that worsen tissue damage.
- The immune response in OA is complex, involving not only macrophage changes but also adaptive immune cells like T cells that contribute to ongoing inflammation in the joint.
- Emerging therapeutic strategies, including Wnt pathway inhibitors and gene therapies, may offer new ways to modify the disease's progression, though challenges in translation to clinical practice persist.
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