We are analyzing https://link.springer.com/article/10.1007/s11010-008-9803-8.

Title:
Oxidative stress mediates cardiac fibrosis by enhancing transforming growth factor-beta1 in hypertensive rats | Molecular and Cellular Biochemistry
Description:
Cardiac fibrosis represented as perivascular/interstial fibrosis occurs in patients with hypertension. Oxidative stress has been demonstrated to contribute to such structural remodeling. The underlying mechanisms, however, remain to be elucidated. Herein, we tested the hypothesis that oxidative stress mediates cardiac fibrogenesis by stimulating transforming growth factor (TGF)-β1 expression, which in turn triggers a series of fibrogenic responses. Sprague–Dawley rats were treated with angiotensin (Ang)II (9 μg/h s) for 4 weeks with/without co-treatment of combined antioxidants, apocynin, and tempol (120 mg/kg/day each, oral). Untreated rats served as controls. Appearance of cardiac oxidative stress and its potential effect on the expression of TGF-β1, population of myofibroblasts, collagen synthesis/degradation, and fibrosis in hearts were examined. Chronic AngII infusion elevated systemic blood pressure (210 ± 5 mmHg). Extensive perivascular and interstitial fibrosis was found in both ventricles, which were co-localized with oxidative stress represented as upregulated NADPH oxidase (gp91phox subunit) expression. Co-treatment with antioxidants led to: (1) markedly decreased cardiac gp91phox; (2) significantly attenuated gene expression of TGF-β1, type-I collagen, and tissue inhibitors of matrix metalloproteinase (TIMP)-I/II in the heart; (3) largely reduced population of myofibroblasts at sites of fibrosis; (4) significantly reduced cardiac collagen volume; (5) and partially suppressed blood pressure (190 ± 4 mmHg). Thus, cardiac oxidative stress promotes the development of cardiac fibrosis by upregulating TGF-β1 expression, which subsequently enhances cardiac collagen synthesis and suppresses collagen degradation in hypertensive rats.
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month download article/chapter perivascular/interstial fibrosis occurs tgf-beta 1 induced upregulating tgf-β1 expression cardiac hypertrophy cardiac fibrosis induced time-dependent expression pattern cardiac oxidative stress renin-angiotensin-aldosterone system salt-sensitive hypertensive rat aldosterone-induced inflammation oxidative stress represented cellular biochemistry aims ventricular pressure overload full article pdf redox-dependent signalling intramyocardial perivascular fibrosis privacy choices/manage cookies upregulated nadph oxidase cardiac cell proliferation collagen synthesis/degradation pressure-independent effects tgf-beta yao sun health science center oxidative stress rat mesangial cells article molecular chronic kidney disease angiotensin-converting enzyme cardiac fibrosis suppresses collagen degradation pressure overload cardiovascular health tissue angiotensin ii progressive kidney fibrosis european economic area 120 mg/kg/day largely reduced population med clin north reactive oxygen species growth factors 1 hypertensive myocardial fibrosis tgf-β1 conditions privacy policy article zhao hepatic stellate cells normal tissue repair growing cultured fibroblasts cardiovascular diseases

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         description:Cardiac fibrosis represented as perivascular/interstial fibrosis occurs in patients with hypertension. Oxidative stress has been demonstrated to contribute to such structural remodeling. The underlying mechanisms, however, remain to be elucidated. Herein, we tested the hypothesis that oxidative stress mediates cardiac fibrogenesis by stimulating transforming growth factor (TGF)-β1 expression, which in turn triggers a series of fibrogenic responses. Sprague–Dawley rats were treated with angiotensin (Ang)II (9 μg/h s) for 4 weeks with/without co-treatment of combined antioxidants, apocynin, and tempol (120 mg/kg/day each, oral). Untreated rats served as controls. Appearance of cardiac oxidative stress and its potential effect on the expression of TGF-β1, population of myofibroblasts, collagen synthesis/degradation, and fibrosis in hearts were examined. Chronic AngII infusion elevated systemic blood pressure (210 ± 5 mmHg). Extensive perivascular and interstitial fibrosis was found in both ventricles, which were co-localized with oxidative stress represented as upregulated NADPH oxidase (gp91phox subunit) expression. Co-treatment with antioxidants led to: (1) markedly decreased cardiac gp91phox; (2) significantly attenuated gene expression of TGF-β1, type-I collagen, and tissue inhibitors of matrix metalloproteinase (TIMP)-I/II in the heart; (3) largely reduced population of myofibroblasts at sites of fibrosis; (4) significantly reduced cardiac collagen volume; (5) and partially suppressed blood pressure (190 ± 4 mmHg). Thus, cardiac oxidative stress promotes the development of cardiac fibrosis by upregulating TGF-β1 expression, which subsequently enhances cardiac collagen synthesis and suppresses collagen degradation in hypertensive rats.
         datePublished:2008-06-26T00:00:00Z
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      description:Cardiac fibrosis represented as perivascular/interstial fibrosis occurs in patients with hypertension. Oxidative stress has been demonstrated to contribute to such structural remodeling. The underlying mechanisms, however, remain to be elucidated. Herein, we tested the hypothesis that oxidative stress mediates cardiac fibrogenesis by stimulating transforming growth factor (TGF)-β1 expression, which in turn triggers a series of fibrogenic responses. Sprague–Dawley rats were treated with angiotensin (Ang)II (9 μg/h s) for 4 weeks with/without co-treatment of combined antioxidants, apocynin, and tempol (120 mg/kg/day each, oral). Untreated rats served as controls. Appearance of cardiac oxidative stress and its potential effect on the expression of TGF-β1, population of myofibroblasts, collagen synthesis/degradation, and fibrosis in hearts were examined. Chronic AngII infusion elevated systemic blood pressure (210 ± 5 mmHg). Extensive perivascular and interstitial fibrosis was found in both ventricles, which were co-localized with oxidative stress represented as upregulated NADPH oxidase (gp91phox subunit) expression. Co-treatment with antioxidants led to: (1) markedly decreased cardiac gp91phox; (2) significantly attenuated gene expression of TGF-β1, type-I collagen, and tissue inhibitors of matrix metalloproteinase (TIMP)-I/II in the heart; (3) largely reduced population of myofibroblasts at sites of fibrosis; (4) significantly reduced cardiac collagen volume; (5) and partially suppressed blood pressure (190 ± 4 mmHg). Thus, cardiac oxidative stress promotes the development of cardiac fibrosis by upregulating TGF-β1 expression, which subsequently enhances cardiac collagen synthesis and suppresses collagen degradation in hypertensive rats.
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