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40
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Text
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URL Address
<a href="http://doi.org/10.3389/fphys.2014.00439" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fphys.2014.00439</a>
Pages
439–439
Volume
5
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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The impact of age-related dysregulation of the angiotensin system on mitochondrial redox balance.
Publisher
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Frontiers in physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
1905-07
Subject
The topic of the resource
aging; mitochondria; angiotensin II; angiotensin II type 1 receptor blockers; frailty; mitochondrial angiotensin system; redox regulation
Creator
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Vajapey Ramya; Rini David; Walston Jeremy; Abadir Peter
Description
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Aging is associated with the accumulation of various deleterious changes in cells. According to the free radical and mitochondrial theory of aging, mitochondria initiate most of the deleterious changes in aging and govern life span. The failure of mitochondrial reduction-oxidation (redox) homeostasis and the formation of excessive free radicals are tightly linked to dysregulation in the Renin Angiotensin System (RAS). A main rate-controlling step in RAS is renin, an enzyme that hydrolyzes angiotensinogen to generate angiotensin I. Angiotensin I is further converted to Angiotensin II (Ang II) by angiotensin-converting enzyme (ACE). Ang II binds with equal affinity to two main angiotensin receptors-type 1 (AT1R) and type 2 (AT2R). The binding of Ang II to AT1R activates NADPH oxidase, which leads to increased generation of cytoplasmic reactive oxygen species (ROS). This Ang II-AT1R-NADPH-ROS signal triggers the opening of mitochondrial KATP channels and mitochondrial ROS production in a positive feedback loop. Furthermore, RAS has been implicated in the decrease of many of ROS scavenging enzymes, thereby leading to detrimental levels of free radicals in the cell. AT2R is less understood, but evidence supports an anti-oxidative and mitochondria-protective function for AT2R. The overlap between age related changes in RAS and mitochondria, and the consequences of this overlap on age-related diseases are quite complex. RAS dysregulation has been implicated in many pathological conditions due to its contribution to mitochondrial dysfunction. Decreased age-related, renal and cardiac mitochondrial dysfunction was seen in patients treated with angiotensin receptor blockers. The aim of this review is to: (a) report the most recent information elucidating the role of RAS in mitochondrial redox hemostasis and (b) discuss the effect of age-related activation of RAS on generation of free radicals.
Identifier
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<a href="http://doi.org/10.3389/fphys.2014.00439" target="_blank" rel="noreferrer noopener">10.3389/fphys.2014.00439</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Abadir Peter
Aging
angiotensin II
angiotensin II type 1 receptor blockers
Frailty
Frontiers in physiology
Mitochondria
mitochondrial angiotensin system
Redox regulation
Rini David
Vajapey Ramya
Walston Jeremy
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.yjmcc.2015.09.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yjmcc.2015.09.001</a>
Pages
14–28
Volume
88
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Overexpressing superoxide dismutase 2 induces a supernormal cardiac function by enhancing redox-dependent mitochondrial function and metabolic dilation.
Publisher
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Journal of molecular and cellular cardiology
Date
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2015
2015-11
Subject
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Adenosine Triphosphate/biosynthesis; Animals; Arterial Pressure/drug effects; Bioenergetics; Blood Flow Velocity/drug effects; Cardiac function; Cardiac/drug effects/*enzymology; Catalase/pharmacology; Echocardiography; Female; Gene Expression; Heart/drug effects/*enzymology; Hydrogen Peroxide/*metabolism/pharmacology; Injections; Intravenous; Male; Metabolic dilation; Mice; Mitochondria; Myocardium/*enzymology; Myocytes; NG-Nitroarginine Methyl Ester/pharmacology; Oxidation-Reduction; Oxygen Consumption/drug effects; Redox regulation; Signal Transduction; Stroke Volume/drug effects; Superoxide dismutase 2 (SOD2); Superoxide Dismutase/*genetics/metabolism; Transgenic; Transgenic mice; Vasodilation/*drug effects
Creator
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Kang Patrick T; Chen Chwen-Lih; Ohanyan Vahagn; Luther Daniel J; Meszaros J Gary; Chilian William M; Chen Yeong-Renn
Description
An account of the resource
During heightened cardiac work, O2 consumption by the heart benefits energy production via mitochondria. However, some electrons leak from the respiratory chain and yield superoxide, which is rapidly metabolized into H2O2 by SOD2. To understand the systemic effects of the metabolic dilator, H2O2, we studied mice with cardiac-specific SOD2 overexpression (SOD2-tg), which increases the H2O2 produced by cardiac mitochondria. Contrast echocardiography was employed to evaluate cardiac function, indicating that SOD2-tg had a significantly greater ejection fraction and a lower mean arterial pressure (MAP) that was partially normalized by intravenous injection of catalase. Norepinephrine-mediated myocardial blood flow (MBF) was significantly enhanced in SOD2-tg mice. Coupling of MBF to the double product (Heart RatexMAP) was increased in SOD2-tg mice, indicating that the metabolic dilator, "spilled" over, inducing systemic vasodilation. The hypothesis that SOD2 overexpression effectively enhances mitochondrial function was further evaluated. Mitochondria of SOD2-tg mice had a decreased state 3 oxygen consumption rate, but maintained the same ATP production flux under the basal and L-NAME treatment conditions, indicating a higher bioenergetic efficiency. SOD2-tg mitochondria produced less superoxide, and had lower redox activity in converting cyclic hydroxylamine to stable nitroxide, and a lower GSSG concentration. EPR analysis of the isolated mitochondria showed a significant decrease in semiquinones at the SOD2-tg Qi site. These results support a more reductive physiological setting in the SOD2-tg murine heart. Cardiac mitochondria exhibited no significant differences in the respiratory control index between WT and SOD2-tg. We conclude that SOD2 overexpression in myocytes enhances mitochondrial function and metabolic vasodilation, leading to a phenotype of supernormal cardiac function.
Identifier
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<a href="http://doi.org/10.1016/j.yjmcc.2015.09.001" target="_blank" rel="noreferrer noopener">10.1016/j.yjmcc.2015.09.001</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2015
Adenosine Triphosphate/biosynthesis
Animals
Arterial Pressure/drug effects
Bioenergetics
Blood Flow Velocity/drug effects
Cardiac function
Cardiac/drug effects/*enzymology
Catalase/pharmacology
Chen Chwen-Lih
Chen Yeong-Renn
Chilian William M
Department of Integrative Medical Sciences
Echocardiography
Female
Gene Expression
Heart/drug effects/*enzymology
Hydrogen Peroxide/*metabolism/pharmacology
Injections
Intravenous
Journal of molecular and cellular cardiology
Kang Patrick T
Luther Daniel J
Male
Meszaros J Gary
Metabolic dilation
Mice
Mitochondria
Myocardium/*enzymology
Myocytes
NEOMED College of Medicine
NG-Nitroarginine Methyl Ester/pharmacology
Ohanyan Vahagn
Oxidation-Reduction
Oxygen Consumption/drug effects
Redox regulation
Signal Transduction
Stroke Volume/drug effects
Superoxide dismutase 2 (SOD2)
Superoxide Dismutase/*genetics/metabolism
Transgenic
Transgenic mice
Vasodilation/*drug effects