Open AccessPhosphoinositide 3-Kinase p110α Is a Master Regulator of Exercise-Induced Cardioprotection and PI3K Gene Therapy Rescues Cardiac Dysfunction
Author(s) -
Kate L. Weeks,
XiaoMing Gao,
XiaoJun Du,
Esther J. H. Boey,
Aya Matsumoto,
Bianca C. Bernardo,
Helen Kiriazis,
Nelly Cemerlang,
Joon Win Tan,
Yow Keat Tham,
Thomas Franke,
Hongwei Qian,
Marie A. Bogoyevitch,
Elizabeth A. Woodcock,
Mark A. Febbraio,
Paul Gregorevic,
Julie R. McMullen
Publication year - 2012
Publication title -
circulation heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 104
eISSN - 1941-3297
pISSN - 1941-3289
DOI - 10.1161/circheartfailure.112.966622
Subject(s) - cardioprotection , medicine , pi3k/akt/mtor pathway , cardiac function curve , pressure overload , heat shock protein , endocrinology , transgene , muscle hypertrophy , protein kinase b , phosphoinositide 3 kinase , heart failure , cardiology , myocardial infarction , biology , microbiology and biotechnology , cardiac hypertrophy , phosphorylation , gene , signal transduction , biochemistry
Numerous molecular and biochemical changes have been linked with the cardioprotective effects of exercise, including increases in antioxidant enzymes, heat shock proteins, and regulators of cardiac myocyte proliferation. However, a master regulator of exercise-induced protection has yet to be identified. Here, we assess whether phosphoinositide 3-kinase (PI3K) p110α is essential for mediating exercise-induced cardioprotection, and if so, whether its activation independent of exercise can restore function of the failing heart.
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