Abstract
Chondrocytes are the sole cellular constituents of normal cartilage. The degeneration and apoptosis of these cells are considered the main cause of osteoarthritis (OA). Previous studies have suggested that the enhancement of autophagy in chondrocytes can delay the progression of osteoarthritis by affecting intracellular metabolic activity, i.e., by regulating the metabolism of nutrients, which can delay cell aging and death. In this review, we explored the relationship between autophagy and chondrocyte metabolism and provided new ideas for the prevention and treatment of OA.
Highlights
Mesochondrium, known as the matrix of cartilage, is produced by the chondrocytes
The degeneration and apoptosis of chondrocytes have been considered the main reasons for the development of OA, given that autophagy aids the prevention of cell apoptosis by affecting the cell metabolism
The rapid increase of fat in β-cells can induce autophagy, while the long-term lipid excess can inhibit autophagy [35]. These results suggest an association between lipid metabolism and the activity of autophagy
Summary
Mesochondrium, known as the matrix of cartilage, is produced by the chondrocytes. The levels of intracellular glucose, amino acids and lipids reflect the state of energy and nutrition in the cell and have a key role in regulating metabolism. The activation of autophagy is very important for maintaining normal viability of chondrocytes in the state of low energy.
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