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Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?

The balance of autophagy, apoptosis and necroptosis is crucial to determine the outcome of the cellular response to cholesterol dysregulation. Cholesterol plays a major role in regulating the properties of cell membranes, especially as regards their fluidity, and the regulation of its biosynthesis i...

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Autores principales: Piscianz, Elisa, Vecchi Brumatti, Liza, Tommasini, Alberto, Marcuzzi, Annalisa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6352582/
https://www.ncbi.nlm.nih.gov/pubmed/30632494
http://dx.doi.org/10.4103/1673-5374.247441
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author Piscianz, Elisa
Vecchi Brumatti, Liza
Tommasini, Alberto
Marcuzzi, Annalisa
author_facet Piscianz, Elisa
Vecchi Brumatti, Liza
Tommasini, Alberto
Marcuzzi, Annalisa
author_sort Piscianz, Elisa
collection PubMed
description The balance of autophagy, apoptosis and necroptosis is crucial to determine the outcome of the cellular response to cholesterol dysregulation. Cholesterol plays a major role in regulating the properties of cell membranes, especially as regards their fluidity, and the regulation of its biosynthesis influences the shape and functions of these membranes. Whilst dietary cholesterol can easily be distributed to most organs, the central nervous system, whose membranes are particularly rich in cholesterol, mainly relies on de novo synthesis. For this reason, defects in the biosynthesis of cholesterol can variably affect the development of central nervous system. Moreover, defective synthesis of cholesterol and its intermediates may reflect both on structural cell anomalies and on the response to inflammatory stimuli. Examples of such disorders include mevalonate kinase deficiency, and Smith-Lemli-Opitz syndrome, due to deficiency in biosynthetic enzymes, and type C Niemann-Pick syndrome, due to altered cholesterol trafficking across cell compartments. Autophagy, as a crucial pathway dedicated to the degradation of cytosolic proteins and organelles, plays an essential role in the maintenance of homeostasis and in the turnover of the cytoplasmic material especially in the presence of imbalances such as those resulting from alteration of cholesterol metabolism. Manipulating the process of autophagy can offer possible strategies for improving neuronal cell viability and function in these genetic disorders.
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spelling pubmed-63525822019-04-01 Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism? Piscianz, Elisa Vecchi Brumatti, Liza Tommasini, Alberto Marcuzzi, Annalisa Neural Regen Res Review The balance of autophagy, apoptosis and necroptosis is crucial to determine the outcome of the cellular response to cholesterol dysregulation. Cholesterol plays a major role in regulating the properties of cell membranes, especially as regards their fluidity, and the regulation of its biosynthesis influences the shape and functions of these membranes. Whilst dietary cholesterol can easily be distributed to most organs, the central nervous system, whose membranes are particularly rich in cholesterol, mainly relies on de novo synthesis. For this reason, defects in the biosynthesis of cholesterol can variably affect the development of central nervous system. Moreover, defective synthesis of cholesterol and its intermediates may reflect both on structural cell anomalies and on the response to inflammatory stimuli. Examples of such disorders include mevalonate kinase deficiency, and Smith-Lemli-Opitz syndrome, due to deficiency in biosynthetic enzymes, and type C Niemann-Pick syndrome, due to altered cholesterol trafficking across cell compartments. Autophagy, as a crucial pathway dedicated to the degradation of cytosolic proteins and organelles, plays an essential role in the maintenance of homeostasis and in the turnover of the cytoplasmic material especially in the presence of imbalances such as those resulting from alteration of cholesterol metabolism. Manipulating the process of autophagy can offer possible strategies for improving neuronal cell viability and function in these genetic disorders. Medknow Publications & Media Pvt Ltd 2019-04 /pmc/articles/PMC6352582/ /pubmed/30632494 http://dx.doi.org/10.4103/1673-5374.247441 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/4.0 This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
spellingShingle Review
Piscianz, Elisa
Vecchi Brumatti, Liza
Tommasini, Alberto
Marcuzzi, Annalisa
Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?
title Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?
title_full Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?
title_fullStr Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?
title_full_unstemmed Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?
title_short Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?
title_sort is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6352582/
https://www.ncbi.nlm.nih.gov/pubmed/30632494
http://dx.doi.org/10.4103/1673-5374.247441
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