BMP-7 counteracts TGF-β1–induced epithelial-to-mesenchymal transition and reverses chronic renal injury

By M. Zeisberg, J. Hanai, H. Sugimoto, T. Mammoto, D. Charytan, F. Strutz, Raghu Kalluri. Nature Medicine, 2003

1,444 citations recorded by the source corpus.

Subfields: Molecular Biology, Nephrology

View Paper: https://www.semanticscholar.org/paper/0e750e6b6254bf06a06f102c186e3e3022b1a0a9

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Citations in the corpus

The ins and outs of the epithelial to mesenchymal transition in health and disease. (2011, methodology): “The TGFβ pathway has also been a target for inhibition using similar strategies as well as treatment with bone morphogenetic protein 7, an endogenous inhibitor of TGF-β signaling, particularly for the treatment of fibrosis (Zeisberg et al. 2003).”
Modern pathogenetic concepts of liver fibrosis suggest stellate cells and TGF-β as major players and therapeutic targets (2006, background): “the administration of BMP-7 in pharmacological doses attenuates the process of fibrosis and accelerates its reversal in kidney [61, 62].”
Inflammation and EMT: an alliance towards organ fibrosis and cancer progression (2009, background): “Treatment with BMP7, an inhibitor of TGF-b1 signalling, is a promising strategy to treat fibrosis as it can reverse TGF-b1induced renal fibrosis in mice (Zeisberg et al, 2003).”
Cellular and molecular mechanisms of renal fibrosis (2011, background): “A large number of studies have demonstrated a potential role of EMT in kidney fibrosis by examining the phenotypic conversion of tubular cells in animal models as well as in renal biopsy samples from patients with CKD”
Diverse Roles of TGF-β/Smads in Renal Fibrosis and Inflammation (2011, background): “It has been reported that TGF-β-activated Smad2/3 to mediate epithelial-mesenchymal transition (EMT) is reversed by addition of human recombinant BPM-7 via the Smad1-depdnent mechanism [28].”
Methylation determines fibroblast activation and fibrogenesis in the kidney (2010, neutral): “To rule out the possibility that Rasal1 hypermethylation is only relevant in the folic acid–induced nephropathy model, we also assessed Rasal1 methylation in the model of nephrotoxic serum nephritis in C57BL/6 mic”