1
40
2
-
Text
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URL Address
<a href="http://doi.org/10.4330/wjc.v2.i12.421" target="_blank" rel="noreferrer noopener">http://doi.org/10.4330/wjc.v2.i12.421</a>
Pages
421–427
Issue
12
Volume
2
Dublin Core
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Title
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Corruption of coronary collateral growth in metabolic syndrome: Role of oxidative stress.
Publisher
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World journal of cardiology
Date
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2010
2010-12
Subject
The topic of the resource
Angiogenesis; Mitochondria; Arteriogenesis; Redox-dependent signaling
Creator
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Pung Yuh Fen; Chilian William M
Description
An account of the resource
The myocardium adapts to ischemic insults in a variety of ways. One adaptation is the phenomenon of acute preconditioning, which can greatly ameliorate ischemic damage. However, this effect wanes within a few hours and does not confer chronic protection. A more chronic adaptation is the so-called second window of preconditioning, which enables protection for a few days. The most potent adaptation invoked by the myocardium to minimize the effects of ischemia is the growth of blood vessels in the heart, angiogenesis and arteriogenesis (collateral growth), which prevent the development of ischemia by enabling flow to a jeopardized region of the heart. This brief review examines the mechanisms underlying angiogenesis and arteriogenesis in the heart. The concept of a redox window, which is an optimal redox state for vascular growth, is discussed along with signaling mechanisms invoked by reactive oxygen species that are stimulated during ischemia-reperfusion. Finally, the review discusses of some of the pathologies, especially the metabolic syndrome, that negatively affect collateral growth through the corruption of redox signaling processes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.4330/wjc.v2.i12.421" target="_blank" rel="noreferrer noopener">10.4330/wjc.v2.i12.421</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).
2010
angiogenesis
Arteriogenesis
Chilian William M
Department of Integrative Medical Sciences
Mitochondria
NEOMED College of Medicine
Pung Yuh Fen
Redox-dependent signaling
World journal of cardiology
-
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/10.1152/ajpheart.00077.2013" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00077.2013</a>
Pages
H1275–1280
Issue
9
Volume
305
Dublin Core
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Title
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The role of mitochondrial bioenergetics and reactive oxygen species in coronary collateral growth.
Publisher
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American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-11
Subject
The topic of the resource
*Collateral Circulation; *Coronary Circulation; *Energy Metabolism; *Neovascularization; angiogenesis; Animals; arteriogenesis; Coronary Vessels/metabolism; Humans; mitochondria; Mitochondria; Mitochondrial Proteins/metabolism; Muscle; Muscle/*metabolism; Myocytes; Oxidative Stress; Phenotype; Physiologic; Reactive Oxygen Species/*metabolism; redox-dependent signaling; Signal Transduction; Smooth; Smooth Muscle/*metabolism; Vascular/*metabolism
Creator
An entity primarily responsible for making the resource
Pung Yuh Fen; Sam Wai Johnn; Hardwick James P; Yin Liya; Ohanyan Vahagn; Logan Suzanna; Di Vincenzo Lola; Chilian William M
Description
An account of the resource
Coronary collateral growth is a process involving coordination between growth factors expressed in response to ischemia and mechanical forces. Underlying this response is proliferation of vascular smooth muscle and endothelial cells, resulting in an enlargement in the caliber of arterial-arterial anastomoses, i.e., a collateral vessel, sometimes as much as an order of magnitude. An integral element of this cell proliferation is the process known as phenotypic switching in which cells of a particular phenotype, e.g., contractile vascular smooth muscle, must change their phenotype to proliferate. Phenotypic switching requires that protein synthesis occurs and different kinase signaling pathways become activated, necessitating energy to make the switch. Moreover, kinases, using ATP to phosphorylate their targets, have an energy requirement themselves. Mitochondria play a key role in the energy production that enables phenotypic switching, but under conditions where mitochondrial energy production is constrained, e.g., mitochondrial oxidative stress, this switch is impaired. In addition, we discuss the potential importance of uncoupling proteins as modulators of mitochondrial reactive oxygen species production and bioenergetics, as well as the role of AMP kinase as an energy sensor upstream of mammalian target of rapamycin, the master regulator of protein synthesis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00077.2013" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00077.2013</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).
*Collateral Circulation
*Coronary Circulation
*Energy Metabolism
*Neovascularization
2013
American journal of physiology. Heart and circulatory physiology
angiogenesis
Animals
Arteriogenesis
Chilian William M
Coronary Vessels/metabolism
Department of Integrative Medical Sciences
Di Vincenzo Lola
Hardwick James P
Humans
Logan Suzanna
Mitochondria
Mitochondrial Proteins/metabolism
Muscle
Muscle/*metabolism
Myocytes
NEOMED College of Medicine
Ohanyan Vahagn
Oxidative Stress
Phenotype
Physiologic
Pung Yuh Fen
Reactive Oxygen Species/*metabolism
Redox-dependent signaling
Sam Wai Johnn
Signal Transduction
Smooth
Smooth Muscle/*metabolism
Vascular/*metabolism
Yin Liya