found that mice with specific Atg5 knockout in the S3 tubular segment exhibited increased cell death 2 h after reperfusion but lower levels of inflammation, tubular senescence, interstitial fibrosis, and superior renal function 30 days after ischemic AKI, indicating that autophagy is a profibrotic factor in a mouse model of renal fibrosis after ischemia [16]. This evidence concerns the gene ATG5 and renal fibrosis.