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Stanford Scientists Discover Arthritis Cartilage Repair
9 Jan
Summary
- A key protein, 15-PGDH, increases with age and disrupts tissue repair.
- Blocking 15-PGDH activated chondrocyte cells for cartilage maintenance.
- Drug inhibitor showed significant cartilage regeneration in mice.

In a significant development for osteoarthritis research, scientists at Stanford University have pinpointed a protein called 15-PGDH as a key factor in age-related cartilage degeneration. This protein, which elevates with age, hinders tissue repair and inflammation control, leading to joint deterioration.
The research demonstrated that inhibiting 15-PGDH can prompt the body's natural chondrocyte cells to maintain and thicken cartilage. This novel approach successfully regenerated cartilage in older mice with damaged knee joints and prevented osteoarthritis development in younger mice with injuries.
This discovery bypasses the need for stem cell therapy, presenting a less invasive method for adult tissue regeneration. Researchers are optimistic that this finding could lead to future human treatments that restore mobility and alleviate the significant unmet medical need for effective osteoarthritis therapies.


