Involvement of Na+/K+-ATPase in hydrogen peroxide-induced hypertrophy in cardiac myocytes

Liu, Lijun; Li, Jie; Liu, Jiang; Yuan, Zuyi; Pierre, Sandrine V.; Qu, Weikai; Zhao, Xiaochen; Xie, Zijian

doi:10.1016/j.freeradbiomed.2006.08.018

Cited by 47 publications

(54 citation statements)

References 54 publications

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“…The mechanism(s) are still unclear. However, pre-treatment with different antioxidants attenuated the ouabain- induced activation of Na/K-ATPase signaling pathways and other related effects [31, 32, 57, 58]. Our studies further demonstrated a positive feedback loop of the Na/K-ATPase signaling and ROS (Fig.…”

Section: The Interplay Of Na/k-atpase and Ros - A Positive-feedback Osupporting

confidence: 61%

Targeting Na/K-ATPase Signaling: A New Approach to Control Oxidative Stress

Liu

Lilly

Shapiro

2018

CPD

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Renal and cardiac function are greatly affected by chronic oxidative stress which can cause many pathophysiological states. The Na/K-ATPase is well-described as an ion pumping enzyme involved in maintaining cellular ion homeostasis; however, in the past two decades, extensive research has been done to understand the signaling function of the Na/K-ATPase and determine its role in physiological and pathophysiological states. Our lab has shown that the Na/K-ATPase signaling cascade can function as an amplifier of reactive oxygen species (ROS) which can be initiated by cardiotonic steroids or increases in ROS. Regulation of systemic oxidative stress by targeting Na/K-ATPase signaling mediated oxidant amplification improves 5/6th partial nephrectomy (PNx) mediated uremic cardiomyopathy, renal sodium handling, as well as ameliorates adipogenesis. This review will present this new concept of Na/K-ATPase signaling mediated oxidant amplification loop and its clinic implication.

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Section: The Interplay Of Na/k-atpase and Ros - A Positive-feedback Osupporting

confidence: 61%

Targeting Na/K-ATPase Signaling: A New Approach to Control Oxidative Stress

Liu

Lilly

Shapiro

2018

CPD

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“…GO (3 milliunits/ml) induces a low and sustained generation of H 2 O 2 (3-5) that can stimulate Src kinase tyrosine phosphorylation (42) and Na/K-ATPase endocytosis (5). NAC is one of the most bioavailable precursors of the reducing agent glutathione (43) and is more effective in reducing direct protein carbonylation (44,45) than traditional reactive carbonyl species scavengers (46).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Reactive Oxygen Species in a Feed-forward Mechanism of Na/K-ATPase-mediated Signaling Transduction

Yan

Shapiro

Haller

et al. 2013

Journal of Biological Chemistry

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162

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“…Hydrogen peroxide directly induced cardiac hypertrophy [57], and antioxidants prevent hypertrophy induced by tumor necrosis factor-α and angiotensin II [58]. A recent clinical investigation showed that a supplemental antioxidant has no beneficial effects on cardiovascular diseases [59]; however, mitochondria-targeted antioxidant MitoQ10 proved effective for endothelial function improvement and cardiac hypertrophy attenuation in the stroke-prone spontaneously hypertensive rat [35].…”

Section: Discussionmentioning

confidence: 99%

Mitochondria-Targeted Antioxidant Prevents Cardiac Dysfunction Induced by Tafazzin Gene Knockdown in Cardiac Myocytes

Harris

Ren

et al. 2014

Oxidative Medicine and Cellular Longevity

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Tafazzin, a mitochondrial acyltransferase, plays an important role in cardiolipin side chain remodeling. Previous studies have shown that dysfunction of tafazzin reduces cardiolipin content, impairs mitochondrial function, and causes dilated cardiomyopathy in Barth syndrome. Reactive oxygen species (ROS) have been implicated in the development of cardiomyopathy and are also the obligated byproducts of mitochondria. We hypothesized that tafazzin knockdown increases ROS production from mitochondria, and a mitochondria-targeted antioxidant prevents tafazzin knockdown induced mitochondrial and cardiac dysfunction. We employed cardiac myocytes transduced with an adenovirus containing tafazzin shRNA as a model to investigate the effects of the mitochondrial antioxidant, mito-Tempo. Knocking down tafazzin decreased steady state levels of cardiolipin and increased mitochondrial ROS. Treatment of cardiac myocytes with mito-Tempo normalized tafazzin knockdown enhanced mitochondrial ROS production and cellular ATP decline. Mito-Tempo also significantly abrogated tafazzin knockdown induced cardiac hypertrophy, contractile dysfunction, and cell death. We conclude that mitochondria-targeted antioxidant prevents cardiac dysfunction induced by tafazzin gene knockdown in cardiac myocytes and suggest mito-Tempo as a potential therapeutic for Barth syndrome and other dilated cardiomyopathies resulting from mitochondrial oxidative stress.

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Involvement of Na+/K+-ATPase in hydrogen peroxide-induced hypertrophy in cardiac myocytes

Cited by 47 publications

References 54 publications

Targeting Na/K-ATPase Signaling: A New Approach to Control Oxidative Stress

Targeting Na/K-ATPase Signaling: A New Approach to Control Oxidative Stress

Involvement of Reactive Oxygen Species in a Feed-forward Mechanism of Na/K-ATPase-mediated Signaling Transduction

Mitochondria-Targeted Antioxidant Prevents Cardiac Dysfunction Induced by Tafazzin Gene Knockdown in Cardiac Myocytes

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