Mary B. Goldring1
1Weill 
Human
  cartilage is complex tissue of matrix proteins varying from superficial to
  deep layers and from loaded to unloaded zones. During OA development normally
  quiescent chondrocytes with low matrix turnover undergo phenotypic modulation
  causing matrix destruction and abnormal repair. We have been investigating
  mechanisms by which GADD45β, a stress response signaling molecule
  involved in cartilage development, and ESE-1, an inflammation-induced
  transcription factor, regulate collagen remodeling during osteoarthritis.
  Studies using human surgical specimens and mouse models of OA will elucidate
  how these factors disrupt cartilage homeostasis, leading to the development
  of targeted therapies that block cartilage damage, promoting effective
  repair.
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