Why the study?
Endothelial activation and inflammatory infiltration contribute to renin-angiotensin-induced cardiac fibrosis, but the specific effects of endothelial cell Nox4 on cardiac fibrosis remain unknown.
Does endothelial Nox4 overexpression prevent Angiotensin II-induced cardiac fibrosis in mice?
Population
Transgenic mice overexpressing endothelial-restricted Nox4 and wild-type littermates
Comparison
Transgenic mice vs wild-type controls subjected to chronic AngII infusion
Design
Animal experimental study
Follow-up
14 days
Authors
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Endothelial Nox4 modulation merits further mechanistic study in fibrosis models; leaves open any clinical relevance in human heart failure.
Does endothelial Nox4 overexpression prevent Angiotensin II-induced cardiac fibrosis in mice?
Endothelial Nox4 overexpression protects against Angiotensin II-induced cardiac fibrosis by inhibiting endothelial cell activation and inflammatory cell recruitment.
Wang et al. (2021) studied this question.
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