How tubular epithelial cells dictate the rate of renal fibrogenesis?

Table 1 Major molecules produced by tubular epithelial cells and involved in renal fibrogenesis

	Role in renal fibrosis	Ref.
Transforming growth factor beta pathway
TGFβ	Pro-fibrotic agent via EMT, activation of myofibroblasts.	[8,15,25-27,30]
CTGF	Trap ligand for TGFβ (promotes its action)	[21,28-31]
BMP7	Anti-Fibrotic agent. Counteracts TGFβ	[14,15]
KCP	Trap ligand for BMP7 (promotes its action)	[13]
Hypoxia pathway
HIF	Promotes fibrosis through the induction of TGFβ, CTGF, PDGF, and PAI-1. Promotes endothelial survival through the induction of VEGF.	[34-36,41-42]
VEGF	Promotes endothelial fenestration, and survival.	[38-40,42,43]
PAI-1	Pro-fibrotic agent. Inhibitis plasmin formation.	[32,33]
Ph
Acidotic pH	Induces EMT, enhances angiotensin 2 and endothelin secretion.	[44,50,52-53]

TGFβ: Transforming growth factor β; CTGF: Connective tissue growth factor; BMP7: Bone morphogenetic protein 7; KCP: Kielin/chordin-like protein; HIF: Hypoxia inducible factor; VEGF: Vascular endothelial growth factor; PAI-1: Type 1 plasminogen activator inhibitor.