Li Zhou

TL;DR: Smad7 is a critical negative regulator of TGF-beta/Smad2/3 and NF-kappaB signalling and plays a negative regulating role in both renal fibrosis and inflammation after UUO, and further support the notion that Smad7 may be a therapeutic agent for kidney diseases.

TL;DR: It is suggested that AA induces TEC death via apoptosis by dephosphorylation of STAT3 and posttranslational activation of p53, supporting the hypothesis that p53 promotes renal injury in acute AAN.

TL;DR: Testing the hypothesis that transforming growth factor (TGF)-beta/Smad3 may be a key pathway leading to chronic AAN found that chronic administration of aristolochic acid (AA) resulted in a severe AAN characterized by progressive renal dysfunction and tubulointerstitial fibrosis including epithelial-mesenchymal transition (EMT).

TL;DR: Mice overexpressing latent TGF-beta1 in the skin were protected against anti-GBM crescentic glomerulonephritis, possibly via Smad 7-mediated inhibition of NF-kappaB-dependent renal inflammation and TGF -beta/Smad2/3-dependent fibrosis.

TL;DR: Investigation of the mechanisms and anti-hepatofibrotic activities of asiatic acid in a rat model of liver fibrosis and in vitro in TGF-beta1-stimulated rat hepatic stellate cell line reveals an essential role for Smad7 in AA-induced anti-fibrotics activities during liver fibritis in vivo and in vivo.