Autophagy is a cellular stress responseto exogenous or endogenous stimuli, mediated by lysosomal removal of damaged or functionally unnecessary organelles. This inhibits cellular apoptosis and enhances the cell survival rate (6,7). Beclin 1, a homolog of the yeast Atg6, is a protein encoded by an autophagy-associated gene. A complex of phosphatidylinositol 3-kinase (PI3K) and Beclin 1 is formed that promotes the formation of autophagosomes, thereby inducing autophagy (8,9). Autophagy is thought to be cell-protective under certain pathological conditions (10,11). In recent years, studies demonstrated that, under low nutrient conditions, apoptosis of cartilage cells was inhibited due to autophagy stimulation (12). These **data** suggested that autophagy may be useful in protecting the loss of cartilage cells, and may provide a novel therapeutic approach for OA (13,14). However, previous studies have primarily been focused on Beclin 1 expression and its effect on chondrocyte autophagy, and the effects of Beclin 1 expression on the apoptosis of chondrocytes and the activity of matrix metalloproteinases (MMPs) has yet to be elucidated (8,12,13). In the present study, the role of Beclin 1 in chondrocyte apoptosis was investigated, as were the effects on ECM metabolism, and their underlying molecular mechanisms.