Key result
Angiotensin II increases reactive oxygen species generation and collagen production in cardiac fibroblasts, which can be blocked by NAD(P)H oxidase inhibitors such as apocynin.
Angiotensin II induces cardiac fibrosis via NAD(P)H oxidase-dependent reactive oxygen species generation, a process that can be completely blocked by the antioxidant apocynin in preclinical models.
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NAD(P)H oxidase inhibition may mitigate fibrosis; leaves open clinical translation from fibroblast models.
Angiotensin II increases the NAD(P)H-dependent superoxide anion production and the intracellular generation of reactive oxygen species in cardiac fibroblasts and apocynin, a NAD(P)H oxidase inhibitor, abrogates this rise. The membrane associated NAD(P)H oxidase complex is the predominant source of superoxide anion and reactive oxygen species generation in angiotensin II-stimulated adult cardiac fibroblasts. Inhibition of this NAD(P)H oxidase complex with apocynin completely blocks the angiotensin II-stimulated collagen production, collagen I and III protein and mRNA expression.
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Paul Lijnen (2011) conducted a review in Cardiac fibrosis. Angiotensin II was evaluated. Angiotensin II increases reactive oxygen species generation and collagen production in cardiac fibroblasts, which can be blocked by NAD(P)H oxidase inhibitors such as apocynin.
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