{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T00:42:55Z","timestamp":1792111375201,"version":"4.4.0"},"reference-count":53,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,2,18]],"date-time":"2013-02-18T00:00:00Z","timestamp":1361145600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Osteoarthritis (OA) and degenerative disc disease (DDD) are similar diseases involving the breakdown of cartilage tissue, and a better understanding of the underlying biochemical processes involved in cartilage degeneration may allow for the development of novel biologic therapies aimed at slowing the disease process. Three members of the fibroblast growth factor (FGF) family, FGF\u20102, FGF\u201018, and FGF\u20108, have been implicated as contributing factors in cartilage homeostasis. The role of FGF\u20102 is controversial in both articular and intervertebral disc (IVD) cartilage as it has been associated with species\u2010 and age\u2010dependent anabolic or catabolic events. Recent evidence suggests that FGF\u20102 selectively activates FGF receptor 1 (FGFR1) to exert catabolic effects in human articular chondrocytes and IVD tissue via upregulation of matrix\u2010degrading enzyme production, inhibition of extracellular matrix (ECM) accumulation and proteoglycan synthesis, and clustering of cells characteristic of arthritic states. FGF\u201018, on the other hand, most likely exerts anabolic effects in human articular chondrocytes by activating the FGFR3 pathway, inducing ECM formation and chondrogenic cell differentiation, and inhibiting cell proliferation. These changes result in dispersed chondrocytes or disc cells surrounded by abundant matrix. The role of FGF\u20108 has recently been identified as a catabolic mediator in rat and rabbit articular cartilage, but its precise biological impact on human adult articular cartilage or IVD tissue remains unknown. The available evidence reveals the promise of FGF\u20102\/FGFR1 antagonists, FGF\u201018\/FGFR3 agonists, and FGF\u20108 antagonists (i.e., anti\u2010FGF\u20108 antibody) as potential therapies to prevent cartilage degeneration and\/or promote cartilage regeneration and repair in the future. J. Cell. Biochem. 114: 735\u2013742, 2013. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcb.24418","type":"journal-article","created":{"date-parts":[[2012,10,11]],"date-time":"2012-10-11T10:50:13Z","timestamp":1349952613000},"page":"735-742","source":"Crossref","is-referenced-by-count":196,"title":["Fibroblast growth factor control of cartilage 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