1
40
2
-
Text
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URL Address
<a href="http://doi.org/10.1136/heartjnl-2012-302920a.154" target="_blank" rel="noreferrer noopener">http://doi.org/10.1136/heartjnl-2012-302920a.154</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
E62-E63
Volume
98
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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
Interference With Akt Signaling In Dyslipidemia Diminishes Myocardial Infarction And Promotes Survival By Inhibiting Oxidative Stress
Publisher
An entity responsible for making the resource available
Heart
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-10
Subject
The topic of the resource
Cardiovascular System & Cardiology
Creator
An entity primarily responsible for making the resource
Ma L N; Kerr B A; West X Z; Malinin N L; Weber M E; Ding L; Somanath P R; Penn M S; Podrez E A; Byzova T V
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1136/heartjnl-2012-302920a.154" target="_blank" rel="noreferrer noopener">10.1136/heartjnl-2012-302920a.154</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Byzova T V
Cardiovascular System & Cardiology
Ding L
heart
Kerr B A
Ma L N
Malinin N L
Penn M S
Podrez E A
Somanath P R
Weber M E
West X Z
-
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/10.1126/scisignal.2003948" target="_blank" rel="noreferrer noopener">http://doi.org/10.1126/scisignal.2003948</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
12-12
Issue
287
Volume
6
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Locate full-text within NEOMED Library's e-journal collections
<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>
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
Interference With Akt Signaling Protects Against Myocardial Infarction And Death By Limiting The Consequences Of Oxidative Stress
Publisher
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Science Signaling
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-08
Subject
The topic of the resource
adhesion molecule-1 expression; Biochemistry & Molecular Biology; cardiac dysfunction; Cell Biology; density-lipoprotein; extends life-span; foam cell-formation; nf-kappa-b; nitric-oxide; oxidized phospholipids; scavenger receptor cd36; sr-bi
Creator
An entity primarily responsible for making the resource
Kerr B A; Ma L N; West X Z; Ding L; Malinin N L; Weber M E; Tischenko M; Goc A; Somanath P R; Penn M S; Podrez E A; Byzova T V
Description
An account of the resource
The intricacy of multiple feedback loops in the pathways downstream of Akt allows this kinase to control multiple cellular processes in the cardiovascular system and precludes inferring consequences of its activation in specific pathological conditions. Akt1, the major Akt isoform in the heart and vasculature, has a protective role in the endothelium during atherosclerosis. However, Akt1 activation may also have detrimental consequences in the cardiovascular system. Mice lacking both the high-density lipoprotein receptor SR-BI (scavenger receptor class B type I) and ApoE (apolipoprotein E), which promotes clearance of remnant lipoproteins, are a model of severe dyslipidemia and spontaneous myocardial infarction. We found that Akt1 was activated in these mice, and this activation correlated with cardiac dysfunction, hypertrophy, and fibrosis; increased infarct area; cholesterol accumulation in macrophages and atherosclerosis; and reduced life span. Akt1 activation was associated with inflammation, oxidative stress, accumulation of oxidized lipids, and increased abundance of CD36, a major sensor of oxidative stress, and these events created a positive feedback loop that exacerbated the consequences of oxidative stress. Genetic deletion of Akt1 in this mouse model resulted in decreased mortality, alleviation of multiple complications of heart disease, and reduced occurrence of spontaneous myocardial infarction. Thus, interference with Akt1 signaling in vivo could be protective and improve survival under dyslipidemic conditions by reducing oxidative stress and responses to oxidized lipids.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1126/scisignal.2003948" target="_blank" rel="noreferrer noopener">10.1126/scisignal.2003948</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2013
adhesion molecule-1 expression
Biochemistry & Molecular Biology
Byzova T V
cardiac dysfunction
Cell Biology
density-lipoprotein
Ding L
extends life-span
foam cell-formation
Goc A
Journal Article or Conference Abstract Publication
Kerr B A
Ma L N
Malinin N L
nf-kappa-b
nitric-oxide
oxidized phospholipids
Penn M S
Podrez E A
scavenger receptor cd36
Science Signaling
Somanath P R
sr-bi
Tischenko M
Weber M E
West X Z