Table 1.
Autophagy of different types of kidney cell and renal fibrosis.
| Animal Models | Kidney Cell | Renal Disease Model | Renal Function | Renal Phenotype | Autophagy Activity | Fibrosis | Ref. |
|---|---|---|---|---|---|---|---|
| Conditional deletion of ATG5 in proximal tubular S3 segments | RTECs | 30 days after ischemia/reperfusion | Improve | Decreased tubular senescence | Decreased | Alleviation of interstitial fibrosis | [147] |
| Conditional deletion of ATG5 in proximal tubular S3 segments | RTECs | 2 hours after ischemia/reperfusion | - | more cell death as well as tubular damage and inflammation | Decreased | - | [147] |
| Kidney proximal tubule-specific knockout of ATG7 | RTECs | Unilateral ureteral obstruction (UUO) | - | Decreased proliferation and activation of myofibroblasts, decreased ECM components accumulation and tubular atrophy, cell apoptosis, nephron loss, interstitial macrophage infiltration and the expression of a profibrotic factor FGF2 were all inhibited | Decreased | Alleviated | [148] |
| PTEC-specific deletion of ATG5 | RTECs | UUO model | - | Robust ECM deposition and increasing number of RTECs arrested at the cell cycle G2/M phase | Decreased | Remarkably interstitial fibrosis | [132, 133, 150] |
| Specific deletion of Atg5 | Podocytes | Aged | Decline | Accumulation of ubiquitinated proteins, ER stress, podocytes loss, massive proteinuria, more vulnerable to glomerular disease | Decreased | Finally resulting in glomerulosclerosis and renal fibrosis | [120] |
| Specifically deletion of Atg5 in podocytes | Podocytes | Diabetic nephropathy (DN) model | Decline | Accelerated diabetes-induced podocytopathy, massive proteinuria | Decreased | Glomerulosclerosis | [161] |
| Specifically deletion of Atg5 | Podocytes | high-fat diet (HFD) -induced diabetic model | Decline | Podocyte loss and podocytes apoptosis, massive proteinuria | Decreased | Glomerulosclerosis | [162] |
| Specifically deletion of Atg5 in GECs, Atg5fl/fl; Cdh5-Cre | Glomerular endothelial cell (GECs) | 10 weeks old | Decline | Mild alterations in the glomerular filtration barrier at baseline, slight dilation of glomerular capillaries, discrete podocyte foot process effacements and loss of glomerular endothelial fenestrations accompanied by endothelial cytoplasmic thickening | Decreased | Glomerulosclerosis | [161] |
| Specifically deletion of Atg5 in GECs, Atg5fl/fl; Cdh5-Cre | Glomerular endothelial cell (GECs) | Diabetes mellitus (DM) | More severe in dilation of glomerular capillaries, endothelial lesions, glomerular basement membrane (GBM) thickening and podocyte foot process broadening and effacement | Decreased | Glomerulosclerosis | [161] | |
| Atg5fl/fl;Tek-Cre, specifically deletion of Atg5 | GECs | - | - | Slightly distended capillary loops accompanied by an accumulation of ROS four weeks after birth, a lobular pattern with thickening of the capillary loops and mesangial matrix expansion eight weeks after birth, and died by twelve weeks of age | Decreased | Glomerulosclerosis | [167] |
| - | Glomerular mesangial cell (GMC) | TGF-β1 | - | Decreased GMC apoptosis and promoting its survival | Increased | Decreased | [169] |
| - | GMC | AGEs | - | GMC senescence | Decrease | Senescence | [172] |
| - | GMC | Ang II | - | GMC senescence | Increase | Senescence | [173] |