PI3Kα is essential for the recovery from Cre/tamoxifen cardiotoxicity and in myocardial insulin signalling but is not required for normal myocardial contractility in the adult heart | Zendy

Brent A. McLean | Zendy; Pavel Zhabyeyev | Zendy; Vaibhav B. Patel | Zendy; Ratnadeep Basu | Zendy; Nirmal Parajuli | Zendy; Jessica DesAulniers | Zendy; Allan G. Murray | Zendy; Zamaneh Kassiri | Zendy; Bart Vanhaesebroeck | Zendy; Gavin Y. Oudit | Zendy

Open Access

PI3Kα is essential for the recovery from Cre/tamoxifen cardiotoxicity and in myocardial insulin signalling but is not required for normal myocardial contractility in the adult heart

Author(s) -

Brent A. McLean,

Pavel Zhabyeyev,

Vaibhav B. Patel,

Ratnadeep Basu,

Nirmal Parajuli,

Jessica DesAulniers,

Allan G. Murray,

Zamaneh Kassiri,

Bart Vanhaesebroeck,

Gavin Y. Oudit

Publication year - 2015

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvv016

Subject(s) - cardiotoxicity , contractility , pi3k/akt/mtor pathway , medicine , tamoxifen , cancer , cardiology , endocrinology , breast cancer , biology , chemotherapy , signal transduction , microbiology and biotechnology

Genetic mouse models have yielded conflicting conclusions about the role of PI3Kα in heart physiology: specifically, the question of whether PI3Kα has a direct role in regulating myocardial contractility. This has led to concerns that PI3K inhibitors currently in clinical trials for cancer may potentiate cardiotoxicity. Here we seek to clarify the role of PI3Kα in normal heart physiology and investigate changes in related signalling pathways.

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