Abstract: As a clinical pathological syndrome, focal segmental glomerulosclerosis （FSGS） is characterized by focal glomerulosclerosis, disappearance of podocyte processes and massive proteinuria. Current researches have confirmed that foot cell injury is a central pathogenetic cause of FSGS. And a growing number of studies have demonstrated that oxidative stress, inflammation and disruption of proximal tubular epithelial cells （PTECs） and glomerular endothelial cells （GECs） contribute to the development of FSGS. In recent years, autophagy has attracted greater attention in various research fields. It proved that autophagy plays an important regulatory role in FSGS, And it provided a novel therapeutic target FSGS. This review focused upon autophagy and its roles in FSGS.