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01.12.2012 | Review | Ausgabe 1/2012 Open Access

Cardiovascular Diabetology 1/2012

Mammalian target of rapamycin signaling in diabetic cardiovascular disease

Zeitschrift:
Cardiovascular Diabetology > Ausgabe 1/2012
Autoren:
Zhao Zhong Chong, Kenneth Maiese
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1475-2840-11-45) contains supplementary material, which is available to authorized users.

Competing interests

The authors have no competing interests.

Authors’ contributions

ZZC and KM drafted the manuscript. ZZC and KM completed the final versions of the manuscript with the incorporation of figures and tables. All authors read and approved the final manuscript.

Abstract

Diabetes mellitus currently affects more than 170 million individuals worldwide and is expected to afflict another 200 million individuals in the next 30 years. Complications of diabetes as a result of oxidant stress affect multiple systems throughout the body, but involvement of the cardiovascular system may be one of the most severe in light of the impact upon cardiac and vascular function that can result in rapid morbidity and mortality for individuals. Given these concerns, the signaling pathways of the mammalian target of rapamycin (mTOR) offer exciting prospects for the development of novel therapies for the cardiovascular complications of diabetes. In the cardiovascular and metabolic systems, mTOR and its multi-protein complexes of TORC1 and TORC2 regulate insulin release and signaling, endothelial cell survival and growth, cardiomyocyte proliferation, resistance to β-cell injury, and cell longevity. Yet, mTOR can, at times, alter insulin signaling and lead to insulin resistance in the cardiovascular system during diabetes mellitus. It is therefore vital to understand the complex relationship mTOR and its downstream pathways hold during metabolic disease in order to develop novel strategies for the complications of diabetes mellitus in the cardiovascular system.
Zusatzmaterial
Authors’ original file for figure 1
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Authors’ original file for figure 2
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Literatur
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