Abstract
Adipokines—in particular, leptin, the forerunner of this superfamily—are receiving increasing attention for their role in exerting both beneficial and harmful actions in musculoskeletal inflammatory diseases. Leptin has been extensively associated with cartilage metabolism and OA. OA human chondrocytes have been shown to produce higher levels of leptin than normal cartilage1, with the pattern of leptin expression related to the level of cartilage destruction2,3. Moreover, elevated leptin levels have been found in serum, IPFP, synovial tissues, and cartilage of OA patients compared with healthy controls4,5.
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