Abstract
Since its discovery in 1994, leptin has been considered as an adipokine with pleiotropic effects. In this review, we summarize the actual information about the impact of this hormone on cartilage metabolism and pathology. Leptin signalling depends on the interaction with leptin receptor LEPR, being the long isoform of the receptor (LEPRb) the one with more efficient intracellular signalling. Chondrocytes express the long isoform of the leptin receptor and in these cells, leptin signalling, alone or in combination with other molecules, induces the expression of pro-inflammatory molecules and cartilage degenerative enzymes. Leptin has been shown to increase the proliferation and activation of immune cells, increasing the severity of immune degenerative cartilage diseases. Leptin expression in serum and synovial fluid are related to degenerative diseases such as osteoarthritis (OA), rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Inhibition of leptin signalling showed to have protective effects in these diseases showing the key role of leptin in cartilage degeneration.
Highlights
Articular cartilage is a highly specialized connective tissue that is found in synovial joints
Mast cells express LEPR and leptin signalling promotes the release of inflammatory mediators or cytokines, such as PGD2 and TNF-α, which are necessary for leptin-induced eosinophilic activation and migration [60]
It is clear that leptin has multiple relevant roles in the body, and many research efforts are driven to elucidate the intricate network among, leptin metabolic disorders, inflammatory diseases, and the immune system
Summary
Articular cartilage is a highly specialized connective tissue that is found in synovial joints It consists of a lubricated thin layer of connective tissue between the articulating bones, allowing almost friction-free movement of the joint. Chondrocytes become dysfunctional and exhibit abnormal behaviour in many joint diseases, increasing the degradation of the ECM and losing the ability to repair the tissue [8]. Diverse studies have shown that hypercholesterolemia, hypertension, and high circulating levels of glucose and insulin play a key role in joint and cartilage homeostasis. Despite this evidence, the mechanisms behind the catabolic and inflammatory process are extraordinarily complex and still poorly defined.
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