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doi: 10.1212/WNL.0b013e3182a55f7f
What stands out most is not simply cartilage regrowth, but the mechanism: targeting an age-associated enzyme (15-PGDH) to reprogram existing chondrocytes toward a younger, regenerative statewithout stem cells
Notably, the repression of lipogenic gene and protein expression and the decreased serum triglyceride levels seen in Gclc L-KO mice were reversed in L-DKO mice (Fig
