mTOR, cardiomyocytes and inflammation in cardiac hypertrophy

Xu, L. and Brink, M.. (2016) mTOR, cardiomyocytes and inflammation in cardiac hypertrophy. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 1863 (7 Pt B). pp. 1894-1903.

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Mammalian target of rapamycin (mTOR) is an evolutionary conserved kinase that senses the nutrient and energy status of cells, the availability of growth factors, stress stimuli and other cellular and environmental cues. It responds by regulating a range of cellular processes related to metabolism and growth in accordance with the available resources and intracellular needs. mTOR has distinct functions depending on its assembly in the structurally distinct multiprotein complexes mTORC1 or mTORC2. Active mTORC1 enhances processes including glycolysis, protein, lipid and nucleotide biosynthesis, and it inhibits autophagy. Reported functions for mTORC2 after growth factor stimulation are very diverse, are tissue and cell-type specific, and include insulin-stimulated glucose transport and enhanced glycogen synthesis. In accordance with its cellular functions, mTOR has been demonstrated to regulate cardiac growth in response to pressure overload and is also known to regulate cells of the immune system. The present manuscript presents recently obtained insights into mechanisms whereby mTOR may change anabolic, catabolic and stress response pathways in cardiomocytes and discusses how mTOR may affect inflammatory cells in the heart during hemodynamic stress. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Division of Physiology > CardioBiology (Brink)
UniBasel Contributors:Brink, Marijke
Item Type:Article, refereed
Article Subtype:Further Journal Contribution
Note:Publication type according to Uni Basel Research Database: Journal item
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Last Modified:20 Jan 2019 19:04
Deposited On:20 Jan 2019 19:04

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