Regulation of cardiac autophagy by insulin-like growth factor 1.

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 )/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.

journal_name

IUBMB Life

journal_title

IUBMB life

authors

Troncoso R,Díaz-Elizondo J,Espinoza SP,Navarro-Marquez MF,Oyarzún AP,Riquelme JA,Garcia-Carvajal I,Díaz-Araya G,García L,Hill JA,Lavandero S

doi

10.1002/iub.1172

subject

Has Abstract

pub_date

2013-07-01 00:00:00

pages

593-601

issue

7

eissn

1521-6543

issn

1521-6551

journal_volume

65

pub_type

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