Table 1.
Selected factors mediating EMC during kidney disease
| Factor | Capacity for production |
Cellular response to acute and chronic injury |
||
| tubule | Fibro/Mes | tubule | fibroblast/mesenchymal cell | |
| TGF-β1 | ++ | ++ |
Acute:
anti-inflammatory Chronic: profibrotic Apoptosis ECM generation Hypertrophy |
Acute:
anti-inflammatory Chronic: profibrotic Proliferation Myofibroblast conversion ECM generation |
| Wnt | + | ++ |
Acute:
repair/regeneration Cell survival/proliferation/progenitor recruitment Chronic: profibrotic Partial EMT (via Snail, Fn, MMP-7) ↑ RAS |
Acute:
injury resolution Apoptosis (via MMP-7) Chronic: profibrotic Myofibroblast conversion ECM generation |
| Shh | +++ | + | No direct effect via canonical pathway |
Chronic:
profibrotic Proliferation Myofibroblast conversion ECM generation |
| HGF | – | ++ |
Acute:
repair/regeneration Reducing tubular injury Chronic: repair/regeneration Tubular recovery Anti-inflammatory |
Acute: unknown Chronic: antifibrotic Antagonizing TGF-β1 Apoptosis ↓ ECM generation |
| CTGF | + | ++ | Same as TGF-β1 (cofactor) | Same as TGF-â1 (cofactor) |
| AngII | ++ | – |
Chronic:
profibrotic ↑ TGF-β1 |
Chronic:
profibrotic ↑ TGF-â1 Proliferation ↑ ECM generation |
PDGF = Platelet-derived growth factor; Fibro/Mes = fibroblast/mesenchymal cell; Fn = fibronectin; AngII = angiotensin II.