title: MTOR overactivation and interrupted autophagy flux in obese hearts: a dicey assembly?
abstract: As a central controller of cell growth, mechanistic target of rapamycin (MTOR) affects an array of biological processes, in particular protein synthesis, autophagy and cardiac homeostasis. Conflicting findings have been seen with regard to the role of MTOR signaling and autophagy in cardiac and adipocyte function under metabolic syndrome. AKT, an essential insulin-signaling molecule upstream of MTOR, participates in the regulation of glucose homeostasis and cardiac metabolism. Akt2 knockout may rescue against high-fat diet-disrupted autophagy flux, en route to cardioprotection. Thus, inhibition of MTOR may serve as a possible avenue to retard pathological cardiac hypertrophy via rescuing interrupted autophagic flux.
authors.affiliation: Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY, USA.
authors.forename: Yingmei
authors.initials: Y
authors.lastname: Zhang
authors.forename: Xihui
authors.initials: X
authors.lastname: Xu
authors.forename: Jun
authors.initials: J
authors.lastname: Ren
mesh_terms: D017667:Adipocytes / Q000473:pathology; D000818:Animals; D001343:Autophagy; D059305:Diet, High-Fat; D004789:Enzyme Activation; D006801:Humans; D051379:Mice; D008954:Models, Biological; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology*; D009765:Obesity / Q000201:enzymology* / Q000473:pathology*; D015398:Signal Transduction; D034421:Sus scrofa; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism*
chemical_list: D058570:TOR Serine-Threonine Kinases
keywords: Akt; MTOR; autophagy; cardiac function; obesity