The Experts below are selected from a list of 15237 Experts worldwide ranked by ideXlab platform
Ajay M. Shah - One of the best experts on this subject based on the ideXlab platform.
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Response to Detailed Aspects of Redox Signaling in Cardiac Physiology and Pathology
Circulation Research, 2013Co-Authors: Joseph R. Burgoyne, Heloise Mongue Din, Philip Eaton, Ajay M. ShahAbstract:We thank Figtree et al1 for their interest in our recent review, “Redox Signaling in Cardiac Physiology and Pathology” published in the journal. The authors point out some additional references to their own work on the Na+–K+ pump that were not included. …
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Redox Signaling in Cardiac Physiology and Pathology
Circulation Research, 2012Co-Authors: Joseph R. Burgoyne, Philip Eaton, Heloise Mongue-din, Ajay M. ShahAbstract:Redox signaling refers to the specific and usually reversible oxidation/reduction modification of molecules involved in cellular signaling pathways. In the heart, redox signaling regulates several physiological processes (eg, excitation-contraction coupling) and is involved in a wide variety of pathophysiological and homoeostatic or stress response pathways. Reactive oxygen species involved in Cardiac redox signaling may derive from many sources, but NADPH oxidases, as dedicated sources of signaling reactive oxygen species, seem to be especially important. An increasing number of specific posttranslational oxidative modifications involved in Cardiac redox signaling are being defined, along with the reactive oxygen species sources that are involved. Here, we review current knowledge on the molecular targets of signaling reactive oxygen species in Cardiac cells and their involvement in Cardiac physiopathology. Advances in this field may allow the development of targeted therapeutic strategies for conditions such as heart failure as opposed to the general antioxidant approaches that have failed to date.
Lori L. Isom - One of the best experts on this subject based on the ideXlab platform.
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Voltage-Gated Sodium Channel β1/β1B Subunits Regulate Cardiac Physiology and PathoPhysiology.
Frontiers in physiology, 2018Co-Authors: Nnamdi Edokobi, Lori L. IsomAbstract:Cardiac myocyte contraction is initiated by a set of intricately orchestrated electrical impulses, collectively known as action potentials (APs). Voltage-gated sodium channels (NaVs) are responsible for the upstroke and propagation of APs in excitable cells, including cardiomyocytes. NaVs consist of a single, pore-forming α subunit and two different β subunits. The β subunits are multifunctional cell adhesion molecules and channel modulators that have cell type and subcellular domain specific functional effects. Variants in SCN1B, the gene encoding the Nav-β1 and -β1B subunits, are linked to atrial and ventricular arrhythmias, e.g., Brugada syndrome, as well as to the early infantile epileptic encephalopathy Dravet syndrome, all of which put patients at risk for sudden death. Evidence over the past two decades has demonstrated that Nav-β1/β1B subunits play critical roles in Cardiac myocyte Physiology, in which they regulate tetrodotoxin-resistant and -sensitive sodium currents, potassium currents, and calcium handling, and that Nav-β1/β1B subunit dysfunction generates substrates for arrhythmias. This review will highlight the role of Nav-β1/β1B subunits in Cardiac Physiology and pathoPhysiology.
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voltage gated sodium channel β1 β1b subunits regulate Cardiac Physiology and pathoPhysiology
Frontiers in Physiology, 2018Co-Authors: Nnamdi Edokobi, Lori L. IsomAbstract:Cardiac myocyte contraction is initiated by a set of intricately orchestrated electrical impulses, collectively known as action potentials (APs). Voltage-gated sodium channels (NaVs) are responsible for the upstroke and propagation of APs in excitable cells, including cardiomyocytes. NaVs consist of a single, pore-forming α subunit and two different β subunits. The β subunits are multifunctional cell adhesion molecules and channel modulators that have cell type and subcellular domain specific functional effects. Variants in SCN1B, the gene encoding the Nav-β1 and -β1B subunits, are linked to atrial and ventricular arrhythmias, e.g., Brugada syndrome, as well as to the early infantile epileptic encephalopathy Dravet syndrome, all of which put patients at risk for sudden death. Evidence over the past two decades has demonstrated that Nav-β1/β1B subunits play critical roles in Cardiac myocyte Physiology, in which they regulate tetrodotoxin-resistant and -sensitive sodium currents, potassium currents, and calcium handling, and that Nav-β1/β1B subunit dysfunction generates substrates for arrhythmias. This review will highlight the role of Nav-β1/β1B subunits in Cardiac Physiology and pathoPhysiology.
Joseph R. Burgoyne - One of the best experts on this subject based on the ideXlab platform.
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Response to Detailed Aspects of Redox Signaling in Cardiac Physiology and Pathology
Circulation Research, 2013Co-Authors: Joseph R. Burgoyne, Heloise Mongue Din, Philip Eaton, Ajay M. ShahAbstract:We thank Figtree et al1 for their interest in our recent review, “Redox Signaling in Cardiac Physiology and Pathology” published in the journal. The authors point out some additional references to their own work on the Na+–K+ pump that were not included. …
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Redox Signaling in Cardiac Physiology and Pathology
Circulation Research, 2012Co-Authors: Joseph R. Burgoyne, Philip Eaton, Heloise Mongue-din, Ajay M. ShahAbstract:Redox signaling refers to the specific and usually reversible oxidation/reduction modification of molecules involved in cellular signaling pathways. In the heart, redox signaling regulates several physiological processes (eg, excitation-contraction coupling) and is involved in a wide variety of pathophysiological and homoeostatic or stress response pathways. Reactive oxygen species involved in Cardiac redox signaling may derive from many sources, but NADPH oxidases, as dedicated sources of signaling reactive oxygen species, seem to be especially important. An increasing number of specific posttranslational oxidative modifications involved in Cardiac redox signaling are being defined, along with the reactive oxygen species sources that are involved. Here, we review current knowledge on the molecular targets of signaling reactive oxygen species in Cardiac cells and their involvement in Cardiac physiopathology. Advances in this field may allow the development of targeted therapeutic strategies for conditions such as heart failure as opposed to the general antioxidant approaches that have failed to date.
Duane J Funk - One of the best experts on this subject based on the ideXlab platform.
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role of the venous return in critical illness and shock part ii shock and mechanical ventilation
Critical Care Medicine, 2013Co-Authors: Duane J Funk, Eric Jacobsoh, Anand KumaAbstract:Objective:To provide a conceptual and clinical review of the Physiology of the venous system as it is related to Cardiac function in health and disease.Data:An integration of venous and Cardiac Physiology under normal conditions, critical illness, and resuscitation.Summary:The usual clinical teachin
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the role of venous return in critical illness and shock part i Physiology
Critical Care Medicine, 2013Co-Authors: Duane J Funk, Eric Jacobsohn, Anand KumarAbstract:Objective:To provide a conceptual and clinical review of the Physiology of the venous system as it is relates to Cardiac function in health and disease.Data:An integration of venous and Cardiac Physiology under normal conditions, critical illness, and resuscitation.Summary:The usual teaching of card
Nnamdi Edokobi - One of the best experts on this subject based on the ideXlab platform.
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Voltage-Gated Sodium Channel β1/β1B Subunits Regulate Cardiac Physiology and PathoPhysiology.
Frontiers in physiology, 2018Co-Authors: Nnamdi Edokobi, Lori L. IsomAbstract:Cardiac myocyte contraction is initiated by a set of intricately orchestrated electrical impulses, collectively known as action potentials (APs). Voltage-gated sodium channels (NaVs) are responsible for the upstroke and propagation of APs in excitable cells, including cardiomyocytes. NaVs consist of a single, pore-forming α subunit and two different β subunits. The β subunits are multifunctional cell adhesion molecules and channel modulators that have cell type and subcellular domain specific functional effects. Variants in SCN1B, the gene encoding the Nav-β1 and -β1B subunits, are linked to atrial and ventricular arrhythmias, e.g., Brugada syndrome, as well as to the early infantile epileptic encephalopathy Dravet syndrome, all of which put patients at risk for sudden death. Evidence over the past two decades has demonstrated that Nav-β1/β1B subunits play critical roles in Cardiac myocyte Physiology, in which they regulate tetrodotoxin-resistant and -sensitive sodium currents, potassium currents, and calcium handling, and that Nav-β1/β1B subunit dysfunction generates substrates for arrhythmias. This review will highlight the role of Nav-β1/β1B subunits in Cardiac Physiology and pathoPhysiology.
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voltage gated sodium channel β1 β1b subunits regulate Cardiac Physiology and pathoPhysiology
Frontiers in Physiology, 2018Co-Authors: Nnamdi Edokobi, Lori L. IsomAbstract:Cardiac myocyte contraction is initiated by a set of intricately orchestrated electrical impulses, collectively known as action potentials (APs). Voltage-gated sodium channels (NaVs) are responsible for the upstroke and propagation of APs in excitable cells, including cardiomyocytes. NaVs consist of a single, pore-forming α subunit and two different β subunits. The β subunits are multifunctional cell adhesion molecules and channel modulators that have cell type and subcellular domain specific functional effects. Variants in SCN1B, the gene encoding the Nav-β1 and -β1B subunits, are linked to atrial and ventricular arrhythmias, e.g., Brugada syndrome, as well as to the early infantile epileptic encephalopathy Dravet syndrome, all of which put patients at risk for sudden death. Evidence over the past two decades has demonstrated that Nav-β1/β1B subunits play critical roles in Cardiac myocyte Physiology, in which they regulate tetrodotoxin-resistant and -sensitive sodium currents, potassium currents, and calcium handling, and that Nav-β1/β1B subunit dysfunction generates substrates for arrhythmias. This review will highlight the role of Nav-β1/β1B subunits in Cardiac Physiology and pathoPhysiology.