Regulation of cardiac autophagy by insulin-like growth factor 1

Authors

  • Rodrigo Troncoso,

    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
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  • Jessica Díaz-Elizondo,

    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
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  • Sandra P. Espinoza,

    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
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  • Mario F. Navarro-Marquez,

    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
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  • Alejandra P. Oyarzún,

    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
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  • Jaime A. Riquelme,

    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
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  • Ivonne Garcia-Carvajal,

    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
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  • Guillermo Díaz-Araya,

    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
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  • Lorena García,

    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
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  • Joseph A. Hill,

    1. Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, TX, USA
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  • Sergio Lavandero

    Corresponding author
    1. Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile
    2. Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, TX, USA
    3. Programa Biología Molecular y Celular, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago, Chile
    • Address for correspondence to: Sergio Lavandero, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Sergio Livingstone 1007, Santiago 838-0492, Chile. Tel: +562-2978-2919. Fax: +562-2978-2912. E-mail: slavander@uchile.cl

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Abstract

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. © 2013 IUBMB Life, 65(7):593–601, 2013.

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