Regulation of cardiac autophagy by insulin-like growth factor 1

Rodrigo Troncoso, Jessica Díaz-Elizondo, Sandra P. Espinoza, Mario F. Navarro-Marquez, Alejandra P. Oyarzún, Jaime A. Riquelme, Ivonne Garcia-Carvajal, Guillermo Díaz-Araya, Lorena García, Joseph A Hill, Sergio Lavandero

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


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)/ Ca2+. The Akt/mTOR and Ras/Raf/ERK signaling arms govern survival in the settings of cardiac stress and hypertrophic growth. By contrast, PLC/InsP3/Ca2+ 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.

Original languageEnglish (US)
Pages (from-to)593-601
Number of pages9
JournalIUBMB life
Issue number7
StatePublished - Jul 2013


  • general bioenergetics
  • signal transduction
  • signaling

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics
  • Clinical Biochemistry
  • Cell Biology


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