Knee osteoarthritis (KOA), the highly prevalent degenerative disease affecting the joint, perpetually devastates the health of the elderly. Of various mechanisms known to participate in KOA etiology, apoptosis of chondrocytes is widely regarded as the primary cause of cartilage degradation. It has been suggested that the induction of autophagy in chondrocytes could potentially prolong the progression of KOA by modulating intracellular metabolic processes, which may be helpful for ameliorating chondrocyte apoptosis and eventual cartilage degeneration. Autophagy, a physiological process characterized by intracellular self-degradation, has been reportedly implicated in various pathologic conditions including KOA. Interestingly, vitamin D has been shown to regulate autophagy in human chondrocytes through multiple pathways, specifically AMPK/mTOR signaling pathway. This observation underscores the potential of vitamin D as a novel approach for restoring the functionality and survivability of chondrocytes in KOA. Supporting vitamin D's clinical significance, previous studies have demonstrated its substantial involvement in the symptoms and irregular joint morphology observed in KOA patients, strengthening potential therapeutic efficacy of vitamin D in treatment of KOA. Herein, the purpose of this review was to determine the mechanisms underlying the multi-processes of vitamin D implicated in autophagy in several cells including chondrocytes, which would bring unique insights into KOA pathogenesis.