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A Stanford University team reported in early 2026 that inhibiting a protein called 15‑prostaglandin dehydrogenase (15‑PGDH) in old mice reversed cartilage loss and improved joint function. The discovery suggests a potential therapy for osteoarthritis, a degenerative joint disease affecting millions.
Background
Osteoarthritis is the most common form of arthritis. It occurs when the smooth cartilage cushioning the ends of bones wears away, causing bone surfaces to rub and leading to pain, stiffness and swelling. The condition typically affects the knees, hips, hands and spine and becomes more common after 55 years of age. Risk factors include ageing, obesity, diabetes, high cholesterol, previous joint injuries and hormonal changes after menopause. There is no cure; treatments focus on pain relief, physical therapy and, in severe cases, joint replacement.
Key findings of the study
- Role of 15‑PGDH: Researchers found that levels of the enzyme 15‑PGDH, which degrades prostaglandin E2 (a molecule important for tissue repair), increase with age. High 15‑PGDH activity impairs cartilage regeneration.
- Drug therapy: Injecting a small‑molecule inhibitor of 15‑PGDH into the knees of old mice allowed hyaline cartilage – the glassy cartilage lining joints – to regrow. Treated mice regained weight‑bearing ability and moved more easily than untreated animals.
- Human relevance: Experiments on cartilage tissue from patients with advanced osteoarthritis showed similar regenerative effects when 15‑PGDH was blocked, suggesting that the therapy could work in humans.
- Preventing injury‑induced osteoarthritis: Inhibiting the enzyme not only reversed existing cartilage loss but also prevented osteoarthritis from developing after a knee injury in mice.
Significance
- First disease‑modifying therapy: Current osteoarthritis treatments treat symptoms. Blocking 15‑PGDH targets the underlying cause by promoting cartilage regeneration, potentially delaying or avoiding the need for joint replacements.
- Aging research: The study highlights how age‑related molecular changes can be reversed, opening avenues for treating other degenerative conditions.
- Next steps: Further research is needed to test safety and efficacy in humans, optimise delivery methods and determine whether long‑term inhibition has side effects.
Source: NDTV