New insights into IGF-1 signaling in the heart.

Rodrigo Troncoso, Cristián Ibarra, Jose Miguel Vicencio, Enrique Jaimovich, Sergio Lavandero

Journal: Trends in endocrinology and metabolism: TEM 2014;25(3):128-37

PMID: 24380833

Full Text on Elsevier Science View on PubMed

Abstract

Insulin-like growth factor 1 (IGF-1) signaling regulates contractility, metabolism, hypertrophy, autophagy, senescence, and apoptosis in the heart. IGF-1 deficiency is associated with an increased risk of cardiovascular disease, whereas cardiac activation of IGF-1 receptor (IGF-1R) protects from the detrimental effects of a high-fat diet and myocardial infarction. IGF-1R activates multiple pathways through its intrinsic tyrosine kinase activity and through coupling to heterotrimeric G protein. These pathways involve classic second messengers, phosphorylation cascades, lipid signaling, Ca(2+) transients, and gene expression. In addition, IGF-1R triggers signaling in different subcellular locations including the plasma membrane, perinuclear T tubules, and also in internalized vesicles. In this review, we provide a fresh and updated view of the complex IGF-1 scenario in the heart, including a critical focus on therapeutic strategies.

Address: Facultad de Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago 838049, Chile; Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Quimicas y Farmaceuticas & Facultad de Medicina, Universidad de Chile, Santiago 838049, Chile.; Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm 17177, Sweden.; Hatter Cardiovascular Institute, University College London, London WC1E 6HX, UK.; Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Quimicas y Farmaceuticas & Facultad de Medicina, Universidad de Chile, Santiago 838049, Chile.; Facultad de Ciencias Quimicas y Farmaceuticas & Facultad Medicina, Universidad de Chile, Santiago 838049, Chile; Centro de Estudios Moleculares de la Célula, Facultad de Ciencias Quimicas y Farmaceuticas & Facultad de Medicina, Universidad de Chile, Santiago 838049, Chile; Department of Internal Medicine (Cardiology Division), University of Texas Southwestern Medical Center, Dallas, TX, 75390-8573, USA. Electronic address: [email protected].

DOI: 10.1016/j.tem.2013.12.002

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MeSH Terms: Calcium, Humans, Myocardial Infarction, Myocardium, Phosphorylation, Receptor, IGF Type 1, Signal Transduction, Stem Cells