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Playing with cardiac "redox switches": the "HNO way" to modulate cardiac function.

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Playing with cardiac "redox switches": the "HNO way" to modulate cardiac function. / Tocchetti, Carlo G; Stanley, Brian A; Murray, Christopher I; Sivakumaran, Vidhya; Donzelli, Sonia; Mancardi, Daniele; Pagliaro, Pasquale; Gao, Wei Dong; van Eyk, Jennifer; Kass, David A; Wink, David A; Paolocci, Nazareno.

in: ANTIOXID REDOX SIGN, Jahrgang 14, Nr. 9, 9, 2011, S. 1687-1698.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Tocchetti, CG, Stanley, BA, Murray, CI, Sivakumaran, V, Donzelli, S, Mancardi, D, Pagliaro, P, Gao, WD, van Eyk, J, Kass, DA, Wink, DA & Paolocci, N 2011, 'Playing with cardiac "redox switches": the "HNO way" to modulate cardiac function.', ANTIOXID REDOX SIGN, Jg. 14, Nr. 9, 9, S. 1687-1698. <http://www.ncbi.nlm.nih.gov/pubmed/21235349?dopt=Citation>

APA

Tocchetti, C. G., Stanley, B. A., Murray, C. I., Sivakumaran, V., Donzelli, S., Mancardi, D., Pagliaro, P., Gao, W. D., van Eyk, J., Kass, D. A., Wink, D. A., & Paolocci, N. (2011). Playing with cardiac "redox switches": the "HNO way" to modulate cardiac function. ANTIOXID REDOX SIGN, 14(9), 1687-1698. [9]. http://www.ncbi.nlm.nih.gov/pubmed/21235349?dopt=Citation

Vancouver

Tocchetti CG, Stanley BA, Murray CI, Sivakumaran V, Donzelli S, Mancardi D et al. Playing with cardiac "redox switches": the "HNO way" to modulate cardiac function. ANTIOXID REDOX SIGN. 2011;14(9):1687-1698. 9.

Bibtex

@article{667c06d0c76241c0a7baca57fa3b6421,
title = "Playing with cardiac {"}redox switches{"}: the {"}HNO way{"} to modulate cardiac function.",
abstract = "The nitric oxide (NO(•)) sibling, nitroxyl or nitrosyl hydride (HNO), is emerging as a molecule whose pharmacological properties include providing functional support to failing hearts. HNO also preconditions myocardial tissue, protecting it against ischemia-reperfusion injury while exerting vascular antiproliferative actions. In this review, HNO's peculiar cardiovascular assets are discussed in light of its unique chemistry that distinguish HNO from NO(•) as well as from reactive oxygen and nitrogen species such as the hydroxyl radical and peroxynitrite. Included here is a discussion of the possible routes of HNO formation in the myocardium and its chemical targets in the heart. HNO has been shown to have positive inotropic/lusitropic effects under normal and congestive heart failure conditions in animal models. The mechanistic intricacies of the beneficial cardiac effects of HNO are examined in cellular models. In contrast to ?-receptor/cyclic adenosine monophosphate/protein kinase A-dependent enhancers of myocardial performance, HNO uses its {"}thiophylic{"} nature as a vehicle to interact with redox switches such as cysteines, which are located in key components of the cardiac electromechanical machinery ruling myocardial function. Here, we will briefly review new features of HNO's cardiovascular effects that when combined with its positive inotropic/lusitropic action may render HNO donors an attractive addition to the current therapeutic armamentarium for treating patients with acutely decompensated congestive heart failure.",
keywords = "Animals, Humans, Models, Biological, Reactive Oxygen Species/metabolism, Nitric Oxide Synthase/metabolism, Oxidation-Reduction, Myocardium/metabolism/pathology, Nitrogen Oxides/*metabolism, Reperfusion Injury/metabolism, Sulfhydryl Compounds/metabolism, Animals, Humans, Models, Biological, Reactive Oxygen Species/metabolism, Nitric Oxide Synthase/metabolism, Oxidation-Reduction, Myocardium/metabolism/pathology, Nitrogen Oxides/*metabolism, Reperfusion Injury/metabolism, Sulfhydryl Compounds/metabolism",
author = "Tocchetti, {Carlo G} and Stanley, {Brian A} and Murray, {Christopher I} and Vidhya Sivakumaran and Sonia Donzelli and Daniele Mancardi and Pasquale Pagliaro and Gao, {Wei Dong} and {van Eyk}, Jennifer and Kass, {David A} and Wink, {David A} and Nazareno Paolocci",
year = "2011",
language = "English",
volume = "14",
pages = "1687--1698",
journal = "ANTIOXID REDOX SIGN",
issn = "1523-0864",
publisher = "Mary Ann Liebert Inc.",
number = "9",

}

RIS

TY - JOUR

T1 - Playing with cardiac "redox switches": the "HNO way" to modulate cardiac function.

AU - Tocchetti, Carlo G

AU - Stanley, Brian A

AU - Murray, Christopher I

AU - Sivakumaran, Vidhya

AU - Donzelli, Sonia

AU - Mancardi, Daniele

AU - Pagliaro, Pasquale

AU - Gao, Wei Dong

AU - van Eyk, Jennifer

AU - Kass, David A

AU - Wink, David A

AU - Paolocci, Nazareno

PY - 2011

Y1 - 2011

N2 - The nitric oxide (NO(•)) sibling, nitroxyl or nitrosyl hydride (HNO), is emerging as a molecule whose pharmacological properties include providing functional support to failing hearts. HNO also preconditions myocardial tissue, protecting it against ischemia-reperfusion injury while exerting vascular antiproliferative actions. In this review, HNO's peculiar cardiovascular assets are discussed in light of its unique chemistry that distinguish HNO from NO(•) as well as from reactive oxygen and nitrogen species such as the hydroxyl radical and peroxynitrite. Included here is a discussion of the possible routes of HNO formation in the myocardium and its chemical targets in the heart. HNO has been shown to have positive inotropic/lusitropic effects under normal and congestive heart failure conditions in animal models. The mechanistic intricacies of the beneficial cardiac effects of HNO are examined in cellular models. In contrast to ?-receptor/cyclic adenosine monophosphate/protein kinase A-dependent enhancers of myocardial performance, HNO uses its "thiophylic" nature as a vehicle to interact with redox switches such as cysteines, which are located in key components of the cardiac electromechanical machinery ruling myocardial function. Here, we will briefly review new features of HNO's cardiovascular effects that when combined with its positive inotropic/lusitropic action may render HNO donors an attractive addition to the current therapeutic armamentarium for treating patients with acutely decompensated congestive heart failure.

AB - The nitric oxide (NO(•)) sibling, nitroxyl or nitrosyl hydride (HNO), is emerging as a molecule whose pharmacological properties include providing functional support to failing hearts. HNO also preconditions myocardial tissue, protecting it against ischemia-reperfusion injury while exerting vascular antiproliferative actions. In this review, HNO's peculiar cardiovascular assets are discussed in light of its unique chemistry that distinguish HNO from NO(•) as well as from reactive oxygen and nitrogen species such as the hydroxyl radical and peroxynitrite. Included here is a discussion of the possible routes of HNO formation in the myocardium and its chemical targets in the heart. HNO has been shown to have positive inotropic/lusitropic effects under normal and congestive heart failure conditions in animal models. The mechanistic intricacies of the beneficial cardiac effects of HNO are examined in cellular models. In contrast to ?-receptor/cyclic adenosine monophosphate/protein kinase A-dependent enhancers of myocardial performance, HNO uses its "thiophylic" nature as a vehicle to interact with redox switches such as cysteines, which are located in key components of the cardiac electromechanical machinery ruling myocardial function. Here, we will briefly review new features of HNO's cardiovascular effects that when combined with its positive inotropic/lusitropic action may render HNO donors an attractive addition to the current therapeutic armamentarium for treating patients with acutely decompensated congestive heart failure.

KW - Animals

KW - Humans

KW - Models, Biological

KW - Reactive Oxygen Species/metabolism

KW - Nitric Oxide Synthase/metabolism

KW - Oxidation-Reduction

KW - Myocardium/metabolism/pathology

KW - Nitrogen Oxides/metabolism

KW - Reperfusion Injury/metabolism

KW - Sulfhydryl Compounds/metabolism

KW - Animals

KW - Humans

KW - Models, Biological

KW - Reactive Oxygen Species/metabolism

KW - Nitric Oxide Synthase/metabolism

KW - Oxidation-Reduction

KW - Myocardium/metabolism/pathology

KW - Nitrogen Oxides/metabolism

KW - Reperfusion Injury/metabolism

KW - Sulfhydryl Compounds/metabolism

M3 - SCORING: Journal article

VL - 14

SP - 1687

EP - 1698

JO - ANTIOXID REDOX SIGN

JF - ANTIOXID REDOX SIGN

SN - 1523-0864

IS - 9

M1 - 9

ER -