ArticleOxidative medicine and cellular longevity2012
Blockade of TGF-β 1 signalling inhibits cardiac NADPH oxidase overactivity in hypertensive rats.
Article in Oxidative medicine and cellular longevity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Gene-Level Regulation of Acupuncture Therapy in Spontaneously Hypertensive Rats: A Whole Transcriptome Analysis.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Therapeutic Potential of Polyphenols in Cardiac Fibrosis.Frontiers in pharmacology · 2018Review
- Gallic Acid Reduces Blood Pressure and Attenuates Oxidative Stress and Cardiac Hypertrophy in Spontaneously Hypertensive Rats.Scientific reports · 2017Article
- TRPC3 Channels in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2017Review
- Zingerone alleviates the delayed ventricular repolarization and AV conduction in diabetes: Effect on cardiac fibrosis and inflammation.PloS one · 2017Article
- Apocynin influence on oxidative stress and cardiac remodeling of spontaneously hypertensive rats with diabetes mellitus.Cardiovascular diabetology · 2016Article
- Fibroblast-to-myofibroblast switch is mediated by NAD(P)H oxidase generated reactive oxygen species.Bioscience reports · 2014Article
- A novel role for SIRT-1 in L-arginine protection against STZ induced myocardial fibrosis in rats.PloS one · 2014Article
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Authors and funding
12 authors at 1 institution in 1 country.
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Abstract
NADPH oxidases constitute a major source of superoxide anion (·O(2)(-)) in hypertension. Several studies suggest an important role of NADPH oxidases in different effects mediated by TGF-β 1. In this study we show that chronic administration of P144, a peptide synthesized from type III TGF-β 1 receptor, significantly reduced the cardiac NADPH oxidase expression and activity as well as in the nitrotyrosine levels observed in control spontaneously hypertensive rats (V-SHR) to levels similar to control normotensive Wistar Kyoto rats. In addition, P144 was also able to reduce the significant increases in the expression of collagen type I protein and mRNA observed in hearts from V-SHR. In addition, positive correlations between collagen expression, NADPH oxidase activity, and nitrotyrosine levels were found in all animals. Finally, TGF-β 1-stimulated Rat-2 exhibited significant increases in NADPH oxidase activity that was inhibited in the presence of P144. It could be concluded that the blockade of TGF-β 1 with P144 inhibited cardiac NADPH oxidase in SHR, thus adding new data to elucidate the involvement of this enzyme in the profibrotic actions of TGF-β 1.
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