A new treatment that blocks an aging-related protein restored lost cartilage in old mice and helped prevent arthritis after knee injuries. Human cartilage samples showed similar signs of regeneration, raising hopes for a future drug that could repair joints instead of replacing them.
Maybe, but if PGE2 signaling is disrupted in non-cartilage tissues, it could promote abnormal growth or inflammation. For example, PGE2 has complex roles in cancer and fibrosis. And if the drug isn’t perfectly specific, it might inhibit other enzymes or pathways. This is because 15-PGDH is active in other tissues (e.g., liver, muscle, bone). Inhibiting it systemically might affect these tissues, though the study suggests localized joint injection could minimize this I suppose…