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, Vol. 14, No. 9, 9, 2011, p. 1687-1698.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -