Table 2.

Protective roles of TGF-β signaling in chronic kidney diseases

Strategy and Results	Disease Model	Reference(s)
Conditional deletion of TβRII in renal interstitial cells significantly reduces collagen production, but does not ameliorate overall renal fibrosis.	UUO, aristolochic acid-induced nephropathy	67
Conditional deletion of Smad2 in renal tubular epithelial cells enhances renal fibrosis.	UUO	58
Overexpression of latent TGF-β1 in keratinocytes reduces renal fibrosis	UUO	28
Overexpression of latent TGF-β1 in keratinocytes protects against glomerular crescentic formation and severe tubulointerstitial damage.	Crescentic glomerulonephritis	29
Overexpression of Smad7 suppresses renal fibrosis, whereas deficiency of Smad7 aggravates the severity of renal fibrosis.	Diabetic nephropathy	8
Smad7 overexpression in kidneys suppresses renal fibrosis, and disruption of Smad7 enhances renal fibrosis.	UUO	14, 46
Smad 7 deficiency aggravates angiotensin II-mediated renal fibrosis, whereas Smad7 treatment prevents progressive renal injury.	Hypertensive nephropathy	51, 52
Smad7 disruption exacerbates nephropathy, whereas Smad7 overexpression in kidneys attenuates nephropathy.	Aristolochic acid-induced nephropathy	15
Conditional deletion of TβRII in renal tubular epithelial cells and renal fibroblasts enhances NF-κB signaling and renal inflammation.	UUO	59
Conditional deletion of Smad4 in renal tubular epithelial cells enhances renal inflammation.	UUO	60
Treatment with autophagy inhibitor 3-methyladenine enhances renal tubular cell apoptosis and tubulointerstitial fibrosis.	UUO	41
Heterozygous deletion in Beclin 1- and LC3b-null mice enhances collagen deposition.	UUO	19, 40
Conditional deletion of Atg5 in podocytes increases susceptibility to renal injury.	Puromycin, adriamycin, LPS	27

UUO, unilateral ureteral obstruction.