Effect of Pressure Overload on Cardioprotection via PI3K-Akt: Comparison of Postconditioning, Insulin, and Pressure Unloading | Zendy

Mahmood S. Mozaffari | Zendy; J. Y. Liu | Zendy; Stephen W. Schaffer | Zendy

Open Access

Effect of Pressure Overload on Cardioprotection via PI3K-Akt: Comparison of Postconditioning, Insulin, and Pressure Unloading

Author(s) -

Mahmood S. Mozaffari,

J. Y. Liu,

Stephen W. Schaffer

Publication year - 2010

Publication title -

american journal of hypertension

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.009

H-Index - 136

eISSN - 1941-7225

pISSN - 0895-7061

DOI - 10.1038/ajh.2010.43

Subject(s) - cardioprotection , protein kinase b , pi3k/akt/mtor pathway , medicine , pressure overload , wortmannin , insulin , endocrinology , gsk 3 , ischemia , signal transduction , biology , muscle hypertrophy , microbiology and biotechnology , cardiac hypertrophy

Postconditioning (PC) and insulin exert cardioprotection by activating phosphatidylinositol-3 kinase (PI3K) signaling. Because pressure overload exacerbates ischemia-reperfusion (IR) injury, we tested the hypothesis that (i) pressure overload attenuates PC- and insulin-induced cardioprotection, an effect caused by reduced PI3K-Akt signaling and (ii) pressure unloading confers cardioprotection comparable to either PC or insulin.

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