Abstract
Tissue fibrosis and vascular disease are hallmarks of systemic sclerosis (SSc). Transforming growth factor β (TGFβ) is a key-player in fibroblast activation and tissue fibrosis in SSc. In contrast to fibrosis, evidence for a role of TGFβ in vascular disease of SSc is scarce. Using a transgenic mouse model with fibroblast-specific expression of a kinase-deficient TGFβ receptor type II, Derrett-Smith and colleagues demonstrate that aberrant TGFβ signaling in fibroblasts might result in activation of vascular smooth muscle cells and architectural changes of the vessel wall of the aorta.
Highlights
Tissue fibrosis and vascular disease are hallmarks of systemic sclerosis (SSc)
Using the TβRIIΔk-fib transgenic mouse model, DerrettSmith and colleagues [1] analyzed a potential role of transforming growth factor β (TGFβ) signaling in the vascular pathogenesis of systemic sclerosis (SSc)
Only few data suggest a role of Transforming growth factor β (TGFβ) in the vascular pathogenesis of SSc
Summary
Tissue fibrosis and vascular disease are hallmarks of systemic sclerosis (SSc). Transforming growth factor β (TGFβ) is a key-player in fibroblast activation and tissue fibrosis in SSc. Using the TβRIIΔk-fib transgenic mouse model, DerrettSmith and colleagues [1] analyzed a potential role of transforming growth factor β (TGFβ) signaling in the vascular pathogenesis of systemic sclerosis (SSc).
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