An Update on the Role of Leptin in the Immuno-Metabolism of Cartilage

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.

Automated summary

Leptin, a adipokine, has significant impact on cartilage metabolism and pathology by inducing the expression of pro-inflammatory molecules and cartilage degenerative enzymes through its signaling pathway involving the long isoform of the leptin receptor (LEPRb). It has been shown that inhibition of leptin signaling can have protective effects in degenerative cartilage diseases such as osteoarthritis, rheumatoid arthritis, and systemic lupus erythematosus. Leptin also plays a key role in increasing the proliferation and activation of immune cells, exacerbating the severity of immune degenerative cartilage diseases.