Cardiac Raptor Ablation Impairs Adaptive Hypertrophy, Alters Metabolic Gene Expression, and Causes Heart Failure in Mice | Zendy

Pankaj Shende | Zendy; Isabelle Plaisance | Zendy; C Morandi | Zendy; Corinne Pellieux | Zendy; Corinne Berthonneche | Zendy; Francesco Zorzato | Zendy; Jaya Krishnan | Zendy; René Lerch | Zendy; Michael N. Hall | Zendy; Markus A. Rüegg | Zendy; Thierry Pedrazzini | Zendy; Marijke Brink | Zendy

Open Access

Cardiac Raptor Ablation Impairs Adaptive Hypertrophy, Alters Metabolic Gene Expression, and Causes Heart Failure in Mice

Author(s) -

Pankaj Shende,

Isabelle Plaisance,

C Morandi,

Corinne Pellieux,

Corinne Berthonneche,

Francesco Zorzato,

Jaya Krishnan,

René Lerch,

Michael N. Hall,

Markus A. Rüegg,

Thierry Pedrazzini,

Marijke Brink

Publication year - 2011

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.110.977066

Subject(s) - mtorc1 , pi3k/akt/mtor pathway , heart failure , medicine , muscle hypertrophy , mtorc2 , endocrinology , mechanistic target of rapamycin , pressure overload , cardiomyopathy , biology , microbiology and biotechnology , signal transduction , cardiac hypertrophy

Cardiac hypertrophy involves growth responses to a variety of stimuli triggered by increased workload. It is an independent risk factor for heart failure and sudden death. Mammalian target of rapamycin (mTOR) plays a key role in cellular growth responses by integrating growth factor and energy status signals. It is found in 2 structurally and functionally distinct multiprotein complexes called mTOR complex (mTORC) 1 and mTORC2. The role of each of these branches of mTOR signaling in the adult heart is currently unknown.

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