title: The intersection between growth factors, autophagy and ER stress: A new target to treat neurodegenerative diseases?
abstract: One of the salient features of most neurodegenerative diseases is the aggregation of specific proteins in the brain. This proteostasis imbalance is proposed as a key event triggering the neurodegenerative cascade. The unfolded protein response (UPR) and autophagy pathways are emerging as critical processes implicated in handling disease-related misfolded proteins. However, in some conditions, perturbations in the buffering capacity of the proteostasis network may be part of the etiology of the disease. Thus, pharmacological or gene therapy strategies to enhance autophagy or UPR responses are becoming an attractive target for disease intervention. Here, we discuss current evidence depicting the complex involvement of autophagy and ER stress in brain diseases. Novel pathways to modulate protein misfolding are discussed including the relation between aging and growth factor signaling. This article is part of a Special Issue entitled SI:Autophagy.
authors.affiliation: Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile; FONDAP Center for Geroscience, Brain Health and Metabolism, Santiago, Chile; Program of Cellular and Molecular Biology, Center for Molecular Studies of the Cell Institute of Biomedical Sciences, University of Chile, Chile.
authors.forename: Paula
authors.initials: P
authors.lastname: Garcia-Huerta
authors.affiliation: Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile; FONDAP Center for Geroscience, Brain Health and Metabolism, Santiago, Chile; Program of Cellular and Molecular Biology, Center for Molecular Studies of the Cell Institute of Biomedical Sciences, University of Chile, Chile.
authors.forename: Paulina
authors.initials: P
authors.lastname: Troncoso-Escudero
authors.affiliation: Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile; FONDAP Center for Geroscience, Brain Health and Metabolism, Santiago, Chile; Neurounion Biomedical Foundation, Santiago, Chile.
authors.forename: Carolina
authors.initials: C
authors.lastname: Jerez
authors.affiliation: Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile; FONDAP Center for Geroscience, Brain Health and Metabolism, Santiago, Chile; Program of Cellular and Molecular Biology, Center for Molecular Studies of the Cell Institute of Biomedical Sciences, University of Chile, Chile; Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA, USA. Electronic address: chetz@med.uchile.cl.
authors.forename: Claudio
authors.initials: C
authors.lastname: Hetz
authors.affiliation: Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile; FONDAP Center for Geroscience, Brain Health and Metabolism, Santiago, Chile; Neurounion Biomedical Foundation, Santiago, Chile. Electronic address: rene.vidal@neurounion.com.
authors.forename: Rene L
authors.initials: RL
authors.lastname: Vidal
mesh_terms: D000818:Animals; D001343:Autophagy; D001921:Brain / Q000378:metabolism*; D059865:Endoplasmic Reticulum Stress; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D019636:Neurodegenerative Diseases / Q000378:metabolism*; D057165:Proteostasis Deficiencies / Q000378:metabolism; D015398:Signal Transduction; D056811:Unfolded Protein Response
chemical_list: D036341:Intercellular Signaling Peptides and Proteins
keywords: Autophagy; ER stress, aggregation, neurodegenerative disease; IGFs; UPR