PMID- 23671040
OWN - NLM
STAT- MEDLINE
DCOM- 20140213
LR  - 20130624
IS  - 1521-6551 (Electronic)
IS  - 1521-6543 (Linking)
VI  - 65
IP  - 7
DP  - 2013 Jul
TI  - Regulation of cardiac autophagy by insulin-like growth factor 1.
PG  - 593-601
LID - 10.1002/iub.1172 [doi]
AB  - Insulin-like growth factor-1 (IGF-1) signaling is a key pathway in the control of 
      cell growth and survival. Three critical nodes in the IGF-1 signaling pathway 
      have been described in cardiomyocytes: protein kinase Akt/mammalian target of 
      rapamycin (mTOR), Ras/Raf/extracellular signal-regulated kinase (ERK), and 
      phospholipase C (PLC)/inositol 1,4,5-triphosphate (InsP3 )/Ca(2+) . The Akt/mTOR 
      and Ras/Raf/ERK signaling arms govern survival in the settings of cardiac stress 
      and hypertrophic growth. By contrast, PLC/InsP3 /Ca(2+) functions to regulate 
      metabolic adaptability and gene transcription. Autophagy is a catabolic process 
      involved in protein degradation, organelle turnover, and nonselective breakdown 
      of cytoplasmic components during nutrient starvation or stress. In the heart, 
      autophagy is observed in a variety of human pathologies, where it can be either 
      adaptive or maladaptive, depending on the context. We proposed the hypothesis 
      that IGF-1 protects the heart by rescuing the mitochondrial metabolism and the 
      energetics state, reducing cell death and controls the potentially exacerbate 
      autophagic response to nutritional stress. In light of the importance of IGF-1 
      and autophagy in the heart, we review here IGF-1 signaling and autophagy 
      regulation in the context of cardiomyocyte nutritional stress.
CI  - Copyright (c) 2013 International Union of Biochemistry and Molecular Biology, Inc.
FAU - Troncoso, Rodrigo
AU  - Troncoso R
AD  - Centro de Estudios Moleculares de la Celula, Facultad de Ciencias Quimicas y 
      Farmaceuticas, Universidad de Chile, Santiago, Chile.
FAU - Diaz-Elizondo, Jessica
AU  - Diaz-Elizondo J
FAU - Espinoza, Sandra P
AU  - Espinoza SP
FAU - Navarro-Marquez, Mario F
AU  - Navarro-Marquez MF
FAU - Oyarzun, Alejandra P
AU  - Oyarzun AP
FAU - Riquelme, Jaime A
AU  - Riquelme JA
FAU - Garcia-Carvajal, Ivonne
AU  - Garcia-Carvajal I
FAU - Diaz-Araya, Guillermo
AU  - Diaz-Araya G
FAU - Garcia, Lorena
AU  - Garcia L
FAU - Hill, Joseph A
AU  - Hill JA
FAU - Lavandero, Sergio
AU  - Lavandero S
LA  - eng
GR  - HL-075173/HL/NHLBI NIH HHS/United States
GR  - HL-080144/HL/NHLBI NIH HHS/United States
GR  - HL-090842/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20130514
PL  - England
TA  - IUBMB Life
JT  - IUBMB life
JID - 100888706
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
SB  - IM
MH  - Autophagy
MH  - Cell Proliferation
MH  - Humans
MH  - Insulin-Like Growth Factor I/*metabolism
MH  - Mitochondria/metabolism
MH  - Myocardium/*metabolism
MH  - Myocytes, Cardiac/*metabolism/physiology
MH  - Signal Transduction
MH  - *Stress, Physiological
EDAT- 2013/05/15 06:00
MHDA- 2014/02/14 06:00
CRDT- 2013/05/15 06:00
PHST- 2013/02/14 00:00 [received]
PHST- 2013/03/22 00:00 [accepted]
PHST- 2013/05/15 06:00 [entrez]
PHST- 2013/05/15 06:00 [pubmed]
PHST- 2014/02/14 06:00 [medline]
AID - 10.1002/iub.1172 [doi]
PST - ppublish
SO  - IUBMB Life. 2013 Jul;65(7):593-601. doi: 10.1002/iub.1172. Epub 2013 May 14.