2008
DOI: 10.1291/hypres.31.325
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Angiotensin II Regulates Cardiac Hypertrophy via Oxidative Stress but Not Antioxidant Enzyme Activities in Experimental Renovascular Hypertension

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Cited by 24 publications
(15 citation statements)
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“…Overall, local Ang II and TGF-β1 are currently recognized as critical mediators of Ang II-induced tissue fibrosis; however, other mediators may include hyperaldosteronism 151 , oxidative stress [152][153][154] , and other proinflammatory cytokines (e.g., C-reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1)). 155,156 Thus, further investigation into mechanisms and pathways contributing to tissue remodeling during states of injury and pathophysiological conditions is needed to determine the best practice to delay, reverse or prevent the loss of tissue structure, function and, ultimately, organ failure.…”
Section: 150mentioning
confidence: 99%
“…Overall, local Ang II and TGF-β1 are currently recognized as critical mediators of Ang II-induced tissue fibrosis; however, other mediators may include hyperaldosteronism 151 , oxidative stress [152][153][154] , and other proinflammatory cytokines (e.g., C-reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1)). 155,156 Thus, further investigation into mechanisms and pathways contributing to tissue remodeling during states of injury and pathophysiological conditions is needed to determine the best practice to delay, reverse or prevent the loss of tissue structure, function and, ultimately, organ failure.…”
Section: 150mentioning
confidence: 99%
“…IV. DISCUSSION As reported before hyperglycemia can activate polyol pathway, NADPH oxidase leading to increased oxidative stress, endothelial dysfunction, proliferation of vascular smooth muscle cells and induction of cellular damage [19][20][21].…”
Section: Kidney Tnf-α and Tgf-β1 Expressionmentioning
confidence: 69%
“…In this model, we previously showed a redox imbalance in the aorta [9] , heart [8] and kidney [21] and oxidative stress generation that contributed in the development of the hypertensive stage. As a consequence, HO-1 was overexpressed in these tissues and exerted a protective response against reactive oxygen species [8,9] . Taking into account these previous findings, the main objective of the present work was to establish the role of the HO system in blood pressure regulation in AC rats.…”
Section: Discussionmentioning
confidence: 98%
“…Polizio et al Pharmacology 2011;87:341-349 342 strate [3] , heavy metals [3,4] , glutathione depletion [5] , UVA radiation [6] , hypoxia [7] , hyperoxia [7] , ischemiareperfusion [7] and hypertension [8,9] .…”
mentioning
confidence: 99%
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