September 6, 2013CirculationOpen Access

Mechanistic Target of Rapamycin Complex 2 Protects the Heart From Ischemic Damage

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Why the study?

Does selectively increasing mTORC2 while inhibiting mTORC1 protect the heart from ischemic damage in preclinical models?

Population

Cultured cardiac myocytes and mouse hearts subjected to conditions that mimic ischemic heart disease

Design

Preclinical

Authors

MVMirko VölkersGerman Cancer Research Center MKMathias H. KonstandinHeart Failure & Transplant SDShirin DoroudgarUniversity of Arizona

Discussion

Member takes

Implication

Hypothesis-generating for mTORC2-biased therapy post-MI; leaves open translation to human ischemic disease.

Structured PICO

Does selectively increasing mTORC2 while inhibiting mTORC1 protect the heart from ischemic damage in preclinical models?

Population

Cultured cardiac myocytes and mouse hearts subjected to conditions that mimic ischemic heart disease (myocardial infarction)

Intervention

Pharmacological and molecular alteration of mTORC1 and mTORC2 signaling (inhibition of both with Torin1, suppression of mTORC2 with Rictor, or inhibition of mTORC1 with PRAS40)

Outcome

Cardiomyocyte apoptosis and tissue damage after myocardial infarctionsurrogate

Selectively increasing mTORC2 while concurrently inhibiting mTORC1 signaling may be a novel therapeutic approach for treating ischemic heart disease.

Cite This Study

Völkers et al. (2013) studied this question.

synapsesocial.com/papers/6a7de9da482b22b9a6ac8b94 https://doi.org/10.1161/circulationaha.113.003638

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