Journal
SKELETAL BIOLOGY AND MEDICINE II: BONE AND CARTILAGE HOMEOSTASIS AND BONE DISEASE
Volume 1240, Issue -, Pages 61-69Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/j.1749-6632.2011.06258.x
Keywords
osteoarthritis; articular cartilage; growth factors; Mmp13; Adamts5
Funding
- National Institutes of Health (NIH) [R01-AR055915, R01-AR054465]
- New York State Department of Health [C024320]
- Empire State Stem Cell Board
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR054465, R01AR055915] Funding Source: NIH RePORTER
- Veterans Affairs [I01BX002647] Funding Source: NIH RePORTER
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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-beta 1, WNT3a, and Indian hedgehog; signaling molecules such as Smads, beta-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.
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