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

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

16 Citas (Scopus)

Resumen

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.

Idioma originalInglés
Páginas (desde-hasta)593-601
Número de páginas9
PublicaciónIUBMB Life
Volumen65
N.º7
DOI
EstadoPublicada - 1 jul 2013
Publicado de forma externa

Áreas temáticas de ASJC Scopus

  • Bioquímica
  • Biología molecular
  • Genética
  • Bioquímica clínica
  • Biología celular

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