Regulation of cardiac autophagy by insulin‐like growth factor 1

作者: Rodrigo Troncoso , Jessica Díaz-Elizondo , Sandra P. Espinoza , Mario F. Navarro-Marquez , Alejandra P. Oyarzún

DOI: 10.1002/IUB.1172

关键词:

摘要: Insulin-like growth factor-1 (IGF-1) signaling is a key pathway in the control of cell and survival. Three critical nodes IGF-1 have been described cardiomyocytes: protein kinase Akt/mammalian target rapamycin (mTOR), Ras/Raf/extracellular signal-regulated (ERK), phospholipase C (PLC)/inositol 1,4,5-triphosphate (InsP3)/Ca2+. The Akt/mTOR Ras/Raf/ERK arms govern survival settings cardiac stress hypertrophic growth. By contrast, PLC/InsP3/Ca2+ functions to regulate metabolic adaptability gene transcription. Autophagy catabolic process involved degradation, organelle turnover, nonselective breakdown cytoplasmic components during nutrient starvation or stress. In heart, autophagy observed variety human pathologies, where it can be either adaptive maladaptive, depending on context. We proposed hypothesis that protects heart by rescuing mitochondrial metabolism energetics state, reducing death controls potentially exacerbate autophagic response nutritional light importance we review here regulation context cardiomyocyte © 2013 IUBMB Life, 65(7):593–601, 2013.

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