NADPH oxidase-dependent redox signaling in human heart failure: Relationship between the left and right ventricle

Nediani, Chiara; Borchi, Elisabetta; Giordano, Carla; Baruzzo, Serena; Ponziani, Vanessa; Sebastiani, Mariangela; Nassi, Paolo; Mugelli, Alessandro; d’Amati, Giulia; Cerbai, Elisabetta

doi:10.1016/j.yjmcc.2007.01.009

Cited by 57 publications

(59 citation statements)

References 39 publications

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“…Work from our group found that NADPH oxidase activity was enhanced in pressure-overload cardiac hypertrophy in association with increased Nox2 oxidase expression in both cardiomyocytes and endothelial cells, and that this paralleled the activation of the redox-sensitive kinases ERK1/2, ERK5 and p38MAPK [55]. It has also been shown that NADPH oxidase subunit expression and activity are increased in the myocardium of human failing hearts [56], [57] and [58], suggesting the importance of this pathway in humans.…”

Section: Cardiac Hypertrophymentioning

confidence: 72%

NADPH oxidase signaling and cardiac myocyte function

Akki

Zhang

Murdoch

et al. 2009

Journal of Molecular and Cellular Cardiology

124

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Section: Cardiac Hypertrophymentioning

confidence: 72%

NADPH oxidase signaling and cardiac myocyte function

Akki

Zhang

Murdoch

et al. 2009

Journal of Molecular and Cellular Cardiology

124

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“…Multiple factors including systemic hypertension, I/R injury, myocardial infarction, and diabetes all contribute to increased systemic and myocardial ROS production (16,23,43). NAD(P)H oxidase is the major enzymatic source for ROS production in cardiomyocytes (18,52), and its activity is increased in human heart failure (20,37). Studies (3,36) indicate that factors such as ANG II, TNF␣, and ␣ 1 -adrenergic receptor agonists, lead to enhanced ROS generation and induce hypertrophy in isolated cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

Adiponectin mediates cardioprotection in oxidative stress-induced cardiac myocyte remodeling

Essick¹,

Ouchi²,

Wilson³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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oxygen species (ROS) induce matrix metalloproteinase (MMP) activity that mediates hypertrophy and cardiac remodeling. Adiponectin (APN), an adipokine, modulates cardiac hypertrophy, but it is unknown if APN inhibits ROS-induced cardiomyocyte remodeling. We tested the hypothesis that APN ameliorates ROS-induced cardiomyocyte remodeling and investigated the mechanisms involved. Cultured adult rat ventricular myocytes (ARVM) were pretreated with recombinant APN (30 g/ml, 18 h) followed by exposure to physiologic concentrations of H2O2 (1-200 M). ARVM hypertrophy was measured by [ 3 H]leucine incorporation and atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) gene expression by RT-PCR. MMP activity was assessed by in-gel zymography. ROS was induced with angiotensin (ANG)-II (3.2 mg·kg Ϫ1 ·day Ϫ1 for 14 days) in wild-type (WT) and APN-deficient (APN-KO) mice. Myocardial MMPs, tissue inhibitors of MMPs (TIMPs), p-AMPK, and p-ERK protein expression were determined. APN significantly decreased H2O2-induced cardiomyocyte hypertrophy by decreasing total protein, protein synthesis, ANF, and BNP expression. H2O2-induced MMP-9 and MMP-2 activities were also significantly diminished by APN. APN significantly increased p-AMPK in both nonstimulated and H2O2-treated ARVM. H 2O2-induced p-ERK activity and NF-B activity were both abrogated by APN pretreatment. ANG II significantly decreased myocardial p-AMPK and increased p-ERK expression in vivo in APN-KO vs. WT mice. ANG II infusion enhanced cardiac fibrosis and MMP-2-to-TIMP-2 and MMP-9-to-TIMP-1 ratios in APN-KO vs. WT mice. Thus APN inhibits ROS-induced cardiomyocyte remodeling by activating AMPK and inhibiting ERK signaling and NF-B activity. Its effects on ROS and ultimately on MMP expression define the protective role of APN against ROSinduced cardiac remodeling. reactive oxygen species; adenosine 5=-monophosphate-activated protein kinase; matrix metalloproteinase; cardiomyocyte hypertrophy

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“…35,36 These include alterations in the activity of redox-sensitive protein kinases, such as SAPK and other MAPKs, which may occur indirectly following inactivation of tyrosine phosphatases or through direct activation; these also include alterations in the activity of transcription factors, including NF-B, AP-1, hypoxia-inducible factor-1, and STATs. We have reported that the phosphorylation of Jnk was increased in the RVLM of CHF rabbits.…”

Section: Discussionmentioning

confidence: 99%

Role of Oxidant Stress on AT1 Receptor Expression in Neurons of Rabbits With Heart Failure and in Cultured Neurons

Gao

Roy

et al. 2008

Circulation Research

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Abstract-We have previously reported that the expression of Angiotensin II (Ang II) type 1 receptors (AT1R) was increased in the rostral ventrolateral medulla (RVLM) of rabbits with chronic heart failure (CHF) and in the RVLM of normal rabbits infused with intracerebroventricular (ICV) Ang II. The present study investigated whether oxidant stress plays a role in Ang II-induced AT1R upregulation and its relationship to the transcription factor activator protein 1 (AP1) in CHF rabbits and in the CATHa neuronal cell line. Key Words: angiotensin ii Ⅲ antioxidant enzymes Ⅲ brain Ⅲ c-jun Ⅲ c-Jun NH2-terminal kinase A ngiotensin II (Ang II), the principle mediator of the renin-angiotensin system, plays a pivotal role in cardiovascular and renal homeostasis. Most of the physiological and pathophysiological effects of Ang II are mediated by the Angiotensin II type 1 receptor (AT1R). The activation of the renin-angiotensin system and the sympathetic nervous system in chronic heart failure (CHF) are critical factors that contribute to the development and progression of CHF in patients. 1,2 Evidence also demonstrates that AT1R blockers, when added to conventional treatment for patients with CHF, are associated with a reduction in morbidity and mortality as well as an improvement in quality of life. 3 Currently, blockade of the renin-angiotensin system has become the primary treatment for patients with CHF. Therefore, a comprehensive understanding of the regulation of the AT1R is necessary for developing new therapies to target this receptor in the setting of CHF.The role of reactive oxygen species (ROS) in the cardiovascular system has been investigated extensively over the past decade. 4 It has been reported that, in the rostral ventrolateral medulla (RVLM), the levels of ROS are elevated in stroke-prone spontaneously hypertensive rats. Scavenging superoxide anion (O 2•Ϫ ) in the RVLM reduces both sympathetic nerve activity and blood pressure. 5 Similar evidence has been provided for rabbits with CHF. 6 Ang II induces a rapid and transient increase in ROS in a wide variety of cell types. 7 Ang II-induced ROS-formation is attenuated by the NADPH oxidase inhibitor diphenyleneiodonium chloride (DPI), suggesting that it is mediated through NADPH Oxidase. 7 In addition, Ang II-induced ROS-formation can also be blocked by losartan, 8 suggesting that AT1R and its downstream pathway are involved.However, the downstream targets of ROS have remained largely unexplored, at least for the regulation of the AT1R. Extracellular administration of nonlethal concentrations of H 2 O 2 has been demonstrated to activate mitogen-activated protein kinase (MAPK) as well as the c-Jun amino-terminal kinase (JNK). 9 Endogenous ROS induced by Ang II has also been shown to activate stress activated protein kinase (SAPK), which can be inhibited by treating cells with Original

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NADPH oxidase-dependent redox signaling in human heart failure: Relationship between the left and right ventricle

Cited by 57 publications

References 39 publications

NADPH oxidase signaling and cardiac myocyte function

NADPH oxidase signaling and cardiac myocyte function

Adiponectin mediates cardioprotection in oxidative stress-induced cardiac myocyte remodeling

Role of Oxidant Stress on AT1 Receptor Expression in Neurons of Rabbits With Heart Failure and in Cultured Neurons

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