1
40
2
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Text
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URL Address
<a href="http://doi.org/10.1007/s00395-016-0547-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-016-0547-4</a>
Pages
29–29
Issue
3
Volume
111
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
A name given to the resource
Impaired coronary metabolic dilation in the metabolic syndrome is linked to mitochondrial dysfunction and mitochondrial DNA damage.
Publisher
An entity responsible for making the resource available
Basic research in cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-05
Subject
The topic of the resource
Animal; Animals; Coronary circulation; Coronary microcirculation; Coronary Vessels/metabolism/*physiopathology; Diabetes; Disease Models; DNA; DNA Damage/physiology; DNA Fragmentation; Metabolic Syndrome/metabolism/*physiopathology; Mitochondria; Mitochondria/*metabolism; Mitochondrial/*metabolism; Obesity; Oxidative Stress/physiology; Rats; Reactive Oxygen Species/metabolism; Vasodilation/physiology; Zucker
Creator
An entity primarily responsible for making the resource
Guarini Giacinta; Kiyooka Takahiko; Ohanyan Vahagn; Pung Yuh Fen; Marzilli Mario; Chen Yeong-Renn; Chen Chwen-Lih; Kang Patrick T; Hardwick James P; Kolz Christopher L; Yin Liya; Wilson Glenn L; Shokolenko Inna; Dobson James G Jr; Fenton Richard; Chilian William M
Description
An account of the resource
Mitochondrial dysfunction in obesity and diabetes can be caused by excessive production of free radicals, which can damage mitochondrial DNA. Because mitochondrial DNA plays a key role in the production of ATP necessary for cardiac work, we hypothesized that mitochondrial dysfunction, induced by mitochondrial DNA damage, uncouples coronary blood flow from cardiac work. Myocardial blood flow (contrast echocardiography) was measured in Zucker lean (ZLN) and obese fatty (ZOF) rats during increased cardiac metabolism (product of heart rate and arterial pressure, i.v. norepinephrine). In ZLN increased metabolism augmented coronary blood flow, but in ZOF metabolic hyperemia was attenuated. Mitochondrial respiration was impaired and ROS production was greater in ZOF than ZLN. These were associated with mitochondrial DNA (mtDNA) damage in ZOF. To determine if coronary metabolic dilation, the hyperemic response induced by heightened cardiac metabolism, is linked to mitochondrial function we introduced recombinant proteins (intravenously or intraperitoneally) in ZLN and ZOF to fragment or repair mtDNA, respectively. Repair of mtDNA damage restored mitochondrial function and metabolic dilation, and reduced ROS production in ZOF; whereas induction of mtDNA damage in ZLN reduced mitochondrial function, increased ROS production, and attenuated metabolic dilation. Adequate metabolic dilation was also associated with the extracellular release of ADP, ATP, and H2O2 by cardiac myocytes; whereas myocytes from rats with impaired dilation released only H2O2. In conclusion, our results suggest that mitochondrial function plays a seminal role in connecting myocardial blood flow to metabolism, and integrity of mtDNA is central to this process.
Identifier
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<a href="http://doi.org/10.1007/s00395-016-0547-4" target="_blank" rel="noreferrer noopener">10.1007/s00395-016-0547-4</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).
2016
Animal
Animals
Basic research in cardiology
Chen Chwen-Lih
Chen Yeong-Renn
Chilian William M
Coronary Circulation
Coronary microcirculation
Coronary Vessels/metabolism/*physiopathology
Department of Integrative Medical Sciences
Diabetes
Disease Models
DNA
DNA Damage/physiology
DNA Fragmentation
Dobson James G Jr
Fenton Richard
Guarini Giacinta
Hardwick James P
Kang Patrick T
Kiyooka Takahiko
Kolz Christopher L
Marzilli Mario
Metabolic Syndrome/metabolism/*physiopathology
Mitochondria
Mitochondria/*metabolism
Mitochondrial/*metabolism
NEOMED College of Medicine
Obesity
Ohanyan Vahagn
Oxidative Stress/physiology
Pung Yuh Fen
Rats
Reactive Oxygen Species/metabolism
Shokolenko Inna
Vasodilation/physiology
Wilson Glenn L
Yin Liya
Zucker
-
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.ijcard.2020.04.074" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ijcard.2020.04.074</a>
ISSN
1874-1754 0167-5273
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.ijcard.2020.04.074" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.ijcard.2020.04.074</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Update Year & Number
June 2020 Update II
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
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
A name given to the resource
Myocardial ischemia: From disease to syndrome.
Publisher
An entity responsible for making the resource available
International journal of cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04-26
Subject
The topic of the resource
Angina; Chronic coronary syndromes; Coronary artery disease; Ischemic heart disease; Microvascular dysfunction
Creator
An entity primarily responsible for making the resource
Marzilli Mario; Crea Filippo; Morrone Doralisa; Bonow Robert O; Brown David L; Camici Paolo G; Chilian William M; DeMaria Anthony; Guarini Giacinta; Huqi Alda; Merz C Noel Bairey; Pepine Carl; Scali Maria Chiara; Weintraub William S; Boden William E
Description
An account of the resource
Although current guidelines on the management of stable coronary artery disease acknowledge that multiple mechanisms may precipitate myocardial ischemia, recommended diagnostic, prognostic and therapeutic algorithms are still focused on obstructive epicardial atherosclerotic lesions, and little progress has been made in identifying management strategies for non-atherosclerotic causes of myocardial ischemia. The purpose of this consensus paper is three-fold: 1) to marshal scientific evidence that obstructive atherosclerosis can co-exist with other mechanisms of ischemic heart disease (IHD); 2) to explore how the awareness of multiple precipitating mechanisms could impact on pre-test probability, provocative test results and treatment strategies; and 3) to stimulate a more comprehensive approach to chronic myocardial ischemic syndromes, consistent with the new understanding of this condition.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.ijcard.2020.04.074" target="_blank" rel="noreferrer noopener">10.1016/j.ijcard.2020.04.074</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
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journalArticle
2020
Angina
Boden William E
Bonow Robert O
Brown David L
Camici Paolo G
Chilian William M
Chronic coronary syndromes
Coronary Artery Disease
Crea Filippo
DeMaria Anthony
Department of Integrative Medical Sciences
Guarini Giacinta
Huqi Alda
International journal of cardiology
Ischemic heart disease
journalArticle
June 2020 Update II
Marzilli Mario
Merz C Noel Bairey
Microvascular dysfunction
Morrone Doralisa
NEOMED College of Medicine
Pepine Carl
Scali Maria Chiara
Weintraub William S