The DOI matches its Crossref record; 93 of the 93 references it cites were found in a registry or an index.
TGF-β signaling in tissue fibrosis: Redox controls, target genes and therapeutic opportunities
Open accessAbstract
During development of TGF-β1-initiated fibroproliferative disorders, NADPH oxidases (NOX family members) generate reactive oxygen species (ROS) resulting in downstream transcription of a subset genes encoding matrix structural elements and profibrotic factors. Prominent among the repertoire of disease-implicated genes is the TGF-β1 target gene encoding the potent profibrotic matricellular protein plasminogen activator inhibitor-1 (PAI-1 or SERPINE1). PAI-1 is the major physiologic inhibitor of the plasmin-based pericellular cascade and a causative factor in the development of vascular thrombotic and fibroproliferative disorders. ROS generation in response to TGF-β1 stimulation is rapid and precedes PAI-1 induction; engagement of non-SMAD (e.g., EGFR, Src kinase, MAP kinases, p53) and SMAD2/3 pathways are both required for PAI-1 expression and are ROS-dependent. Recent findings suggest a novel role for p53 in TGF-β1-induced PAI-1 transcription that involves ROS generation and p53/SMAD interactions. Targeting ROS and ROS-activated cellular events is likely to have therapeutic implications in the management of fibrotic disorders, particularly in the context of prolonged TGF-β signaling.
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Cites
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Metadata
- Authors
- Samarakoon, R., Overstreet, J. M., & Higgins, P. J.
- Venue
- Cellular Signalling
- Publisher
- Elsevier BV
- Published
- 2013-01
- Volume
- 25
- Issue
- 1
- Pages
- 264-268
- ISSN
- 0898-6568 (ISSN-L)
- OpenAlex
- W2009358874
- Cited by
- 332
- References
- 93
- FWCI
- 9.18
- Type
- journal article
- Language
- en
- Open access
- green
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