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PI3K(p110α) Protects Against Myocardial Infarction-Induced Heart Failure
Author(s) -
Ruby C.Y. Lin,
Kate L. Weeks,
XiaoMing Gao,
Rohan B. H. Williams,
Bianca C. Bernardo,
Helen Kiriazis,
Vance B. Matthews,
Elizabeth A. Woodcock,
Russell D. Bouwman,
Janelle P. Mollica,
H. J. L. Speirs,
Ian W. Dawes,
Roger J. Daly,
Tetsuo Shioi,
Seigo Izumo,
Mark A. Febbraio,
XiaoJun Du,
Julie R. McMullen
Publication year - 2010
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.109.201988
Subject(s) - pi3k/akt/mtor pathway , heart failure , myocardial infarction , medicine , cardiac function curve , cardiology , endocrinology , biology , microbiology and biotechnology , signal transduction
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).

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