Key result
Angiotensin II activates the Smad signaling system in vascular cells in vivo and in vitro independently of TGF-beta, leading to CTGF and extracellular matrix overexpression.
Population
Wistar rats and growth-arrested vascular smooth muscle cells
Design
Preclinical
Authors
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Ang II-Smad activation may represent a novel fibrosis target; animal data leave open human relevance and require prospective validation.
Angiotensin II activates the profibrotic Smad signaling pathway in vascular cells independently of TGF-beta, revealing a novel mechanism for Ang II-induced vascular fibrosis.
Rodríguez‐Vita et al. (2005) studied Vascular fibrosis. Angiotensin II was evaluated on Smad pathway activation and CTGF/ECM overexpression. Angiotensin II activates the Smad signaling system in vascular cells in vivo and in vitro independently of TGF-beta, leading to CTGF and extracellular matrix overexpression.
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