Key result
Endothelial human ET-1 overexpression induces vascular remodeling and dysfunction via NAD(P)H oxidase activation.
Why the study?
The direct nonhemodynamic effects of endothelium-restricted human preproET-1 overexpression on vascular remodeling and endothelial function were unclear.
Does endothelium-restricted human preproET-1 overexpression cause structural remodeling and endothelial dysfunction in a murine model?
Does endothelium-restricted human preproET-1 overexpression cause structural remodeling and endothelial dysfunction in a murine model?
Endothelium-restricted overexpression of human ET-1 in a new murine model directly causes vascular remodeling and endothelial dysfunction, partly via NAD(P)H oxidase activation.
Hypothesis-generating for ET-1 in human vascular disease; leaves open clinical translation from this murine model.
In this new murine model of endothelium-restricted human preproET-1 overexpression, ET-1 caused structural remodeling and endothelial dysfunction of resistance vessels, consistent with a direct nonhemodynamic effect of ET-1 on the vasculature, at least in part through the activation of vascular NAD(P)H oxidase.
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Amiri et al. (2004) studied this question. Endothelium-restricted overexpression of human endothelin-1 caused structural remodeling and endothelial dysfunction in resistance vessels via vascular NAD(P)H oxidase activation.
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