TGF-β1 and angiotensin networking in cardiac remodeling
By S. Rosenkranz. 2004
640 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d3ef60cf87a4f11d585e1c2b017cdfe5a2fbcb73
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cardiology and Cardiovascular Medicine
- Nikolaos G. Frangogiannis
- H. Ruskoaho
- Virpi Talman
- C. Feghali-Bostwick
- N. Turner
- Marcin Bujak
- Ryan T. Kendall
- K. Porter
In Molecular Biology
- Nikolaos G. Frangogiannis
- H. Ruskoaho
- Virpi Talman
- C. Feghali-Bostwick
- Wei Chen
- N. Turner
- Marcin Bujak
- Ryan T. Kendall
Citations in the corpus
- The role of TGF-β Signaling in Myocardial Infarction and Cardiac Remodeling (2007, background): “The RAS is markedly activated in response to hemodynamic overload and local generation of angiotensin II directlyinducescellularresponsesinbothcardiomyocytesand interstitial cells [ 65 ].”
- Transforming Growth Factor (TGF)-β signaling in cardiac remodeling (2010, background): “Extensive evidence suggests a direct link between the RAS system and TGF-β, indicating that TGF-β1 acts downstream of angiotensin II [65].”
- Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. (2010, neutral): “matrix proteins (Rosenkranz, 2004; Khan & Sheppard, 2006).”
- Fibroblasts in fibrosis: novel roles and mediators (2014, background): “Although the phenomenon is not well characterized in most tissues, AngII is known to promote TGFβ-mediated cardiac remodeling (Rosenkranz, 2004) and the fibrosis observed in left ventricular cardiac hypertrophy (Rosenkranz, 2004).”
- Cardiac fibrosis in myocardial infarction—from repair and remodeling to regeneration (2016, background): “…receptor-mediated up-regulation of TGF-β1 expression, angiotensin-converting enzyme 1 (ACE1) inhibitors and AT1 receptor blockers (ARBs) unsurprisingly inhibit cardiac remodeling and fibrosis in various experimental models (reviewed in Rosenkranz 2004; Porter and Turner 2009; Weber et al. 2013).”
- Cardiac fibroblasts: at the heart of myocardial remodeling. (2009, background): “It is clear that the RAS and TGF-β play essentially independent and overlapping roles in the progression of myocardial remodeling (Rosenkranz, 2004).”