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Autophagy in endothelial cells and tumor angiogenesis
In mammalian cells, autophagy is the major pathway for the degradation and recycling of obsolete and potentially noxious cytoplasmic materials, including proteins, lipids, and whole organelles, through the lysosomes. Autophagy maintains cellular and tissue homeostasis and provides a mechanism to ada...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6460396/ https://www.ncbi.nlm.nih.gov/pubmed/30692642 http://dx.doi.org/10.1038/s41418-019-0287-8 |
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author | Schaaf, Marco B. Houbaert, Diede Meçe, Odeta Agostinis, Patrizia |
author_facet | Schaaf, Marco B. Houbaert, Diede Meçe, Odeta Agostinis, Patrizia |
author_sort | Schaaf, Marco B. |
collection | PubMed |
description | In mammalian cells, autophagy is the major pathway for the degradation and recycling of obsolete and potentially noxious cytoplasmic materials, including proteins, lipids, and whole organelles, through the lysosomes. Autophagy maintains cellular and tissue homeostasis and provides a mechanism to adapt to extracellular cues and metabolic stressors. Emerging evidence unravels a critical function of autophagy in endothelial cells (ECs), the major components of the blood vasculature, which delivers nutrients and oxygen to the parenchymal tissue. EC-intrinsic autophagy modulates the response of ECs to various metabolic stressors and has a fundamental role in redox homeostasis and EC plasticity. In recent years moreover, genetic evidence suggests that autophagy regulates pathological angiogenesis, a hallmark of solid tumors. In the hypoxic, nutrient-deprived, and pro-angiogenic tumor microenvironment, heightened autophagy in the blood vessels is emerging as a critical mechanism enabling ECs to dynamically accommodate their higher bioenergetics demands to the extracellular environment and connect with other components of the tumor stroma through paracrine signaling. In this review, we provide an overview of the major cellular mechanisms regulated by autophagy in ECs and discuss their potential role in tumor angiogenesis, tumor growth, and response to anticancer therapy. |
format | Online Article Text |
id | pubmed-6460396 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-64603962019-06-25 Autophagy in endothelial cells and tumor angiogenesis Schaaf, Marco B. Houbaert, Diede Meçe, Odeta Agostinis, Patrizia Cell Death Differ Review Article In mammalian cells, autophagy is the major pathway for the degradation and recycling of obsolete and potentially noxious cytoplasmic materials, including proteins, lipids, and whole organelles, through the lysosomes. Autophagy maintains cellular and tissue homeostasis and provides a mechanism to adapt to extracellular cues and metabolic stressors. Emerging evidence unravels a critical function of autophagy in endothelial cells (ECs), the major components of the blood vasculature, which delivers nutrients and oxygen to the parenchymal tissue. EC-intrinsic autophagy modulates the response of ECs to various metabolic stressors and has a fundamental role in redox homeostasis and EC plasticity. In recent years moreover, genetic evidence suggests that autophagy regulates pathological angiogenesis, a hallmark of solid tumors. In the hypoxic, nutrient-deprived, and pro-angiogenic tumor microenvironment, heightened autophagy in the blood vessels is emerging as a critical mechanism enabling ECs to dynamically accommodate their higher bioenergetics demands to the extracellular environment and connect with other components of the tumor stroma through paracrine signaling. In this review, we provide an overview of the major cellular mechanisms regulated by autophagy in ECs and discuss their potential role in tumor angiogenesis, tumor growth, and response to anticancer therapy. Nature Publishing Group UK 2019-01-28 2019-04 /pmc/articles/PMC6460396/ /pubmed/30692642 http://dx.doi.org/10.1038/s41418-019-0287-8 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Review Article Schaaf, Marco B. Houbaert, Diede Meçe, Odeta Agostinis, Patrizia Autophagy in endothelial cells and tumor angiogenesis |
title | Autophagy in endothelial cells and tumor angiogenesis |
title_full | Autophagy in endothelial cells and tumor angiogenesis |
title_fullStr | Autophagy in endothelial cells and tumor angiogenesis |
title_full_unstemmed | Autophagy in endothelial cells and tumor angiogenesis |
title_short | Autophagy in endothelial cells and tumor angiogenesis |
title_sort | autophagy in endothelial cells and tumor angiogenesis |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6460396/ https://www.ncbi.nlm.nih.gov/pubmed/30692642 http://dx.doi.org/10.1038/s41418-019-0287-8 |
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