en.Wedoany.com Reported - Researchers at Stanford University have promoted the repair of articular cartilage in animal experiments by inhibiting the activity of the 15-PGDH enzyme, with the relevant findings published in the journal Science. This discovery offers a new approach for treating osteoarthritis that differs from existing therapies.
The self-repair capacity of articular cartilage is extremely limited, which has long made osteoarthritis—a condition affecting hundreds of millions of people worldwide—an incurable disease. Current treatments are mainly limited to alleviating pain, slowing disease progression, or performing joint replacement in the end stage. The research team focused on the 15-PGDH enzyme, which is involved in the breakdown of prostaglandins—signaling molecules related to tissue repair. They observed that the level of this enzyme in articular cartilage increases with age, leading them to hypothesize that it may limit the regenerative capacity of cartilage.
To test this hypothesis, the researchers blocked the activity of 15-PGDH in elderly mice. The results showed that the experimental animals had increased articular cartilage thickness and improved tissue structure. In a post-traumatic osteoarthritis model, this intervention also protected the joints from further damage, and signs of pain in the animals were reduced.
Analysis of the mechanism of action revealed that blocking the enzyme activity did not work through a stem cell pathway but instead altered the behavior of existing chondrocytes (cartilage cells). The number of cells characteristic of damaged tissue decreased, and cells actively synthesizing healthy cartilage components became dominant. The research team described this process as a "rejuvenation" of the cellular program.
Currently, the research remains at the animal experiment stage, and there is still a considerable distance from developing a new drug. It is unclear whether this effect can be maintained long-term, or whether sustained inhibition of 15-PGDH might cause side effects. Nevertheless, the study has attracted academic attention because it attempts to restore the self-repair capacity of articular cartilage rather than merely combating symptoms. If the results can be replicated in humans, it could lead to a novel therapy that both delays joint destruction and helps repair the joint.
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