Clinical impact of myocardial mTORC1 activation in nonischemic dilated cardiomyopathy

Journal of Molecular and Cellular Cardiology

Volumn 91, Issue , 2016, Pages 6-9

  Yano, Toshiyuki ^a   Shimoshige, Shinya ^a   Miki, Takayuki ^a   Tanno, Masaya ^a   Mochizuki, Atsushi ^a   Fujito, Takefumi ^a   Yuda, Satoshi ^a   Muranaka, Atsuko ^a   Ogasawara, Makoto ^a   Hashimoto, Akiyoshi ^a   Tsuchihashi, Kazufumi ^a   Miura, Tetsuji ^a  

^a SAPPORO MEDICAL UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

Angiotensin; Dilated cardiomyopathy; Endomyocardial biopsy; Heart failure; MTOR; Ribosomal protein S6

Indexed keywords

ANGIOTENSIN RECEPTOR ANTAGONIST; DIPEPTIDYL CARBOXYPEPTIDASE INHIBITOR; MAMMALIAN TARGET OF RAPAMYCIN COMPLEX 1; PROTEIN S6; S6 KINASE; MECHANISTIC TARGET OF RAPAMYCIN COMPLEX 1; MTOR PROTEIN, HUMAN; MULTIPROTEIN COMPLEX; PHOSPHOPROTEIN; TARGET OF RAPAMYCIN KINASE;

ADULT; ARTICLE; BRUGADA SYNDROME; CONGESTIVE CARDIOMYOPATHY; CONTROLLED STUDY; DISEASE COURSE; ENZYME ACTIVATION; EVENT FREE SURVIVAL; FEMALE; FOLLOW UP; HEART FAILURE; HEART LEFT VENTRICLE EJECTION FRACTION; HEART MUSCLE BIOPSY; HEART MUSCLE FIBROSIS; HUMAN; HUMAN CELL; HUMAN TISSUE; IMMUNOHISTOCHEMISTRY; MAJOR CLINICAL STUDY; MALE; NONISCHEMIC DILATED CARDIOMYOPATHY; PRIORITY JOURNAL; PROTEIN FUNCTION; RETROSPECTIVE STUDY; SIGNAL TRANSDUCTION; TREND STUDY; AGONISTS; ANIMAL; BIOPSY; CARDIAC MUSCLE; CARDIOMYOPATHY, DILATED; DRUG EFFECTS; ENDOCARDIUM; ENZYMOLOGY; FIBROSIS; GENE EXPRESSION; GENETICS; HEART VENTRICLE; METABOLISM; MIDDLE AGED; MORTALITY; PATHOLOGY; SURVIVAL ANALYSIS;

ADULT; ANGIOTENSIN RECEPTOR ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; ANIMALS; BIOPSY; BRUGADA SYNDROME; CARDIOMYOPATHY, DILATED; DISEASE PROGRESSION; ENDOCARDIUM; ENZYME ACTIVATION; FEMALE; FIBROSIS; GENE EXPRESSION; HEART FAILURE; HEART VENTRICLES; HUMANS; MALE; MIDDLE AGED; MULTIPROTEIN COMPLEXES; MYOCARDIUM; PHOSPHOPROTEINS; RETROSPECTIVE STUDIES; RIBOSOMAL PROTEIN S6 KINASES; RIBOSOMAL PROTEIN S6 KINASES, 70-KDA; SURVIVAL ANALYSIS; TOR SERINE-THREONINE KINASES;

EID: 84952930644     PISSN: 00222828     EISSN: 10958584     Source Type: Journal    
DOI: 10.1016/j.yjmcc.2015.12.022     Document Type: Article

References (15)

1. Bracho-Valdés I., Moreno-Alvarez P., Valencia-Martínez I., Robles-Molina E., Chávez-Vargas L., Vázquez-Prado J. mTORC1- and mTORC2-interacting proteins keep their multifunctional partners focused. IUBMB Life 2011, 63:896-914.
2. Yano T., Ferlito M., Aponte A., Kuno A., Miura T., Murphy E., et al. Pivotal role of mTORC2 and involvement of ribosomal protein S6 in cardioprotective signaling. Circ. Res. 2014, 114:1268-1280.
3. Zhang D., Contu R., Latronico M.V., Zhang J., Rizzi R., Catalucci D., et al. MTORC1 regulates cardiac function and myocyte survival through 4E-BP1 inhibition in mice. J. Clin. Invest. 2010, 120:2805-2816.
4. Shende P., Plaisance I., Morandi C., Pellieux C., Berthonneche C., Zorzato F., et al. Cardiac raptor ablation impairs adaptive hypertrophy, alters metabolic gene expression, and causes heart failure in mice. Circulation 2011, 123:1073-1082.
5. McMullen J.R., Sherwood M.C., Tarnavski O., Zhang L., Dorfman A.L., Shioi T., et al. Inhibition of mTOR signaling with rapamycin regresses established cardiac hypertrophy induced by pressure overload. Circulation 2004, 109:3050-3055.
6. Choi J.C., Muchir A., Wu W., Iwata S., Homma S., Morrow J.P., et al. Temsirolimus activates autophagy and ameliorates cardiomyopathy caused by lamin A/C gene mutation. Sci. Transl. Med. 2012, 4. (144ra102).
7. Bibee K.P., Cheng Y.J., Ching J.K., Marsh J.N., Li A.J., Keeling R.M., et al. Rapamycin nanoparticles target defective autophagy in muscular dystrophy to enhance both strength and cardiac function. FASEB J. 2014, 28:2047-2061.
8. Koyama M., Yano T., Kikuchi K., Miura T. Everolimus-responsive dilated cardiomyopathy in tuberous sclerosis. Eur. Heart J. 2015, 36:2338.
9. Hansen D., Wens I., Vandenabeele F., Verboven K., Eijnde B.O. Altered signaling for mitochondrial and myofibrillar biogenesis in skeletal muscles of multiple sclerosis patients. Transl. Res. 2015, 166:70-79.
10. Kendall R.T., Lee M.H., Pleasant D.L., Robinson K., Kuppuswamy D., McDermott P.J., et al. Arrestin-dependent angiotensin AT1 receptor signaling regulates Akt and mTor-mediated protein synthesis. J. Biol. Chem. 2014, 289:26155-26166.
11. Sansbury B.E., DeMartino A.M., Xie Z., Brooks A.C., Brainard R.E., Watson L.J., et al. Metabolomic analysis of pressure-overloaded and infarcted mouse hearts. Circ. Heart Fail. 2014, 7:634-642.
12. Hein S., Arnon E., Kostin S., Schönburg M., Elsässer A., Polyakova V., et al. Progression from compensated hypertrophy to failure in the pressure-overloaded human heart: structural deterioration and compensatory mechanisms. Circulation 2003, 107:984-991.
13. Nakai A., Yamaguchi O., Takeda T., Higuchi Y., Hikoso S., Taniike M., et al. The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress. Nat. Med. 2007, 13:619-624.
14. Liu Q., Qiu J., Liang M., Golinski J., van Leyen K., Jung J.E., et al. Akt and mTOR mediate programmed necrosis in neurons. Cell Death Dis. 2014, 5.
15. Lian H., Ma Y., Feng J., Dong W., Yang Q., Lu D., et al. Heparin-binding EGF-like growth factor induces heart interstitial fibrosis via an Akt/mTor/p70s6k pathway. PLoS One 2012, 7.