Recent progress in understanding molecular mechanisms of cartilage degeneration during osteoarthritis

Meina Wang, Jie Shen, Hongting Jin, Hee Jeong Im, John Sandy, Di Chen

Research output: Contribution to journalReview articlepeer-review

146 Scopus citations


Osteoarthritis (OA) is a highly prevalent disease affecting more than 20% of American adults. Predispositions include joint injury, heredity, obesity, and aging. Biomechanical alterations are commonly involved. However, the molecular mechanisms of this disease are complex, and there is currently no effective disease-modifying treatment. The initiation and progression of OA subtypes is a complex process that at the molecular level probably involves many cell types, signaling pathways, and changes in extracellular matrix. Ex vivo studies with tissue derived from OA patients and in vivo studies with mutant mice have suggested that pathways involving receptor ligands such as TGF-β1, WNT3a, and Indian hedgehog; signaling molecules such as Smads, β-catenin, and HIF-2a; and peptidases such as MMP13 and ADAMTS4/5 are probably involved to some degree. This review focuses on molecular mechanisms of OA development related to recent findings.

Original languageEnglish
Pages (from-to)61-69
Number of pages9
JournalAnnals of the New York Academy of Sciences
Issue number1
StatePublished - Dec 2011


  • Adamts5
  • Articular cartilage
  • Growth factors
  • Mmp13
  • Osteoarthritis


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