Potential Therapeutic Targets for Cardiac Fibrosis: TGF&bgr;, Angiotensin, Endothelin, CCN2, and PDGF, Partners in Fibroblast Activation
By A. Leask. Circulation Research, 2010
677 citations recorded by the source corpus.
Subfields: Cancer Research, Cardiology and Cardiovascular Medicine, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/660a89ea9658f08c7727854eae6c3676dfbbfc81
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In Cancer Research
In Cardiology and Cardiovascular Medicine
In Molecular Biology
Citations in the corpus
- Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis. (2017, positive): “TGF-β is considered a “master” cytokine/growth factor produced within injured or diseased tissues, where it activates fibroblasts and facilitates ECM production (15, 16).”
- Cardiac fibrosis in myocardial infarction—from repair and remodeling to regeneration (2016, background): “ET-1 is a potent pro-fibrotic mediator that seems to act downstream of TGF-β and Ang II, as both of them induce its secretion (Leask 2010; Kong et al. 2014).”
- Transforming Growth Factor (TGF)-β signaling in cardiac remodeling (2010, background): “Beyond its direct effects on the remodeling heart, TGF-β may also act by inducing expression of downstream effectors, such as CTGF and endothelin [61].”