rdf:type |
|
lifeskim:mentions |
umls-concept:C0018801,
umls-concept:C0020792,
umls-concept:C0035696,
umls-concept:C0044602,
umls-concept:C0285761,
umls-concept:C1101610,
umls-concept:C1150481,
umls-concept:C1368105,
umls-concept:C1424600,
umls-concept:C1451005,
umls-concept:C1522564,
umls-concept:C1705325,
umls-concept:C2003941
|
pubmed:issue |
4
|
pubmed:dateCreated |
2010-3-18
|
pubmed:abstractText |
Myocardial infarction (MI) is a serious complication of atherosclerosis associated with increasing mortality attributable to heart failure. Activation of phosphoinositide 3-kinase [PI3K(p110 alpha)] is considered a new strategy for the treatment of heart failure. However, whether PI3K(p110 alpha) provides protection in a setting of MI is unknown, and PI3K(p110 alpha) is difficult to target because it has multiple actions in numerous cell types. The goal of this study was to assess whether PI3K(p110 alpha) is beneficial in a setting of MI and, if so, to identify cardiac-selective microRNA and mRNA that mediate the protective properties of PI3K(p110 alpha).
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
1524-4636
|
pubmed:author |
pubmed-author:BernardoBianca CBC,
pubmed-author:BouwmanRussell DRD,
pubmed-author:DalyRoger JRJ,
pubmed-author:DawesIan WIW,
pubmed-author:DuXiao-JunXJ,
pubmed-author:FebbraioMark AMA,
pubmed-author:GaoXiao-MingXM,
pubmed-author:IzumoSeigoS,
pubmed-author:KiriazisHelenH,
pubmed-author:LinRuby C YRC,
pubmed-author:MatthewsVance BVB,
pubmed-author:McMullenJulie RJR,
pubmed-author:MollicaJanelle PJP,
pubmed-author:ShioiTetsuoT,
pubmed-author:SpeirsHelen JHJ,
pubmed-author:WeeksKate LKL,
pubmed-author:WilliamsRohan B HRB,
pubmed-author:WoodcockElizabeth AEA
|
pubmed:issnType |
Electronic
|
pubmed:volume |
30
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
724-32
|
pubmed:dateRevised |
2010-11-18
|
pubmed:meshHeading |
pubmed-meshheading:20237330-Animals,
pubmed-meshheading:20237330-Disease Models, Animal,
pubmed-meshheading:20237330-Gene Expression Profiling,
pubmed-meshheading:20237330-Heart Failure,
pubmed-meshheading:20237330-Mice,
pubmed-meshheading:20237330-Mice, Inbred C57BL,
pubmed-meshheading:20237330-Mice, Knockout,
pubmed-meshheading:20237330-Mice, Transgenic,
pubmed-meshheading:20237330-MicroRNAs,
pubmed-meshheading:20237330-Myocardial Infarction,
pubmed-meshheading:20237330-Myocardium,
pubmed-meshheading:20237330-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:20237330-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:20237330-Proteins,
pubmed-meshheading:20237330-RNA, Messenger,
pubmed-meshheading:20237330-Time Factors,
pubmed-meshheading:20237330-Ventricular Function, Left,
pubmed-meshheading:20237330-Ventricular Pressure
|
pubmed:year |
2010
|
pubmed:articleTitle |
PI3K(p110 alpha) protects against myocardial infarction-induced heart failure: identification of PI3K-regulated miRNA and mRNA.
|
pubmed:affiliation |
Ramaciotti Centre for Gene Function Analysis, University of New South Wales, Randwick, Australia.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|