Table 2 ∣.

Effects of autophagy or mitophagy defects on AKI and kidney interstitial fibrosis

Animal model	Targeted tissues	Disease model	Kidney phenotype	Refs
Atg5fl/fl; Kap–Cre	Proximal tubules	Cisplatin and IRI	Increased sensitivity to AKI	57,71
Atg7fl/fl; Pepck–Cre	Proximal tubules	Cisplatin, IRI and LPS	Increased sensitivity to AKI	70,74
Atg5fl/fl; Pax8–rtTA; TetO–Cre	Entire kidney tubules	IRI	Increased sensitivity to AKI	43
Pink1 and Park2 single or double knockout	Global	Cisplatin, IRI, contrast agent	Increased sensitivity to AKI	77,88,90
Atg7fl/fl; Pepck–Cre	Proximal tubules	UUO	Reduced kidney fibrosis, fibroblast proliferation and activation, tubular atrophy, apoptosis, interstitial macrophage infiltration and production of pro-fibrotic factors	108
Atg5fl/fl; GGT:: Ert2–Cre	S3 segment of proximal tubules	IRI	Reduced interstitial fibrosis and tubular senescence and superior kidney function 30 days after AKI	102
Map1lc3a knockout or hemizygous deletion of Becn1	Global	UUO	Increased collagen deposition and TGFβ1 levels in obstructed kidney	118
Atg5fl/fl; Kap–Cre	Proximal tubules	UUO	Increased interstitial fibrosis and cell cycle arrest at the G2/M phase	119
Atg7 deletion	Distal tubules	UUO	Increased tubulointerstitial fibrosis, accumulation of damaged mitochondria, expression of NLRP3 inflammasome, IL-1β and caspase 1	123
Hif1afl/fl; Pax8–rtTA; TetO–Cre	Proximal tubules	IRI	Reduced autophagy in proximal tubules accompanied by increased tubular injury, interstitial fibrosis and functional damage to the kidney	105

AKI, acute kidney injury; IRI, ischaemia–reperfusion injury; LPS, lipopolysaccharide; TGF-β1, transforming growth factor β1; UUO, unilateral ureteric obstruction.