TGF‐β signaling and the fibrotic response
By A. Leask, David J. Abraham. The FASEB Journal, 2004
2,119 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/22232983af3a43c5102d5cd5125e782c4d0810d5
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- Nikolaos G. Frangogiannis
- M. Dobaczewski
- A. Elmarakby
- A. Biernacka
- Søren Bentzen
- A. Ljubimov
- Kevin K. Kim
- Y. Kanwar
Citations in the corpus
- Relationship between oxidative stress and inflammatory cytokines in diabetic nephropathy. (2012, background): “Connective tissue growth factor (CTGF) is a highly profibrogenic molecule which is overexpressed in many fibrotic lesions [83,84].”
- Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury (2010, unknown): “TGF-β1 is a well-established principal driver of fibrosis via promotion of fibroblast proliferation, extracellular matrix synthesis and inhibition of collagenases in multiple organ”
- Progress in corneal wound healing (2015, background): “This temporary ECM appears to be accumulated by a TGF-βdependent mechanism (Leask and Abraham, 2004).”
- TGF-β signaling in fibrosis (2011, background): “TGF-b signaling pathways in fibrosis Animal model experiments have suggested an important in vivo role for TGF-b in the pathogenesis of fibrotic conditions (Leask and Abraham 2004; Pohlers et al. 2009).”