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The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review
Chondrocytes are the sole cellular constituents of normal cartilage. The degeneration and apoptosis of these cells are considered the main cause of osteoarthritis (OA). Previous studies have suggested that the enhancement of autophagy in chondrocytes can delay the progression of osteoarthritis by af...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6487163/ https://www.ncbi.nlm.nih.gov/pubmed/31111057 http://dx.doi.org/10.1155/2019/5171602 |
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author | Luo, Pan Gao, Fuqiang Niu, Dongsheng Sun, Xichun Song, Qiang Guo, Chongjun Liang, Yuqi Sun, Wei |
author_facet | Luo, Pan Gao, Fuqiang Niu, Dongsheng Sun, Xichun Song, Qiang Guo, Chongjun Liang, Yuqi Sun, Wei |
author_sort | Luo, Pan |
collection | PubMed |
description | Chondrocytes are the sole cellular constituents of normal cartilage. The degeneration and apoptosis of these cells are considered the main cause of osteoarthritis (OA). Previous studies have suggested that the enhancement of autophagy in chondrocytes can delay the progression of osteoarthritis by affecting intracellular metabolic activity, i.e., by regulating the metabolism of nutrients, which can delay cell aging and death. In this review, we explored the relationship between autophagy and chondrocyte metabolism and provided new ideas for the prevention and treatment of OA. |
format | Online Article Text |
id | pubmed-6487163 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-64871632019-05-20 The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review Luo, Pan Gao, Fuqiang Niu, Dongsheng Sun, Xichun Song, Qiang Guo, Chongjun Liang, Yuqi Sun, Wei Biomed Res Int Review Article Chondrocytes are the sole cellular constituents of normal cartilage. The degeneration and apoptosis of these cells are considered the main cause of osteoarthritis (OA). Previous studies have suggested that the enhancement of autophagy in chondrocytes can delay the progression of osteoarthritis by affecting intracellular metabolic activity, i.e., by regulating the metabolism of nutrients, which can delay cell aging and death. In this review, we explored the relationship between autophagy and chondrocyte metabolism and provided new ideas for the prevention and treatment of OA. Hindawi 2019-04-14 /pmc/articles/PMC6487163/ /pubmed/31111057 http://dx.doi.org/10.1155/2019/5171602 Text en Copyright © 2019 Pan Luo et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Luo, Pan Gao, Fuqiang Niu, Dongsheng Sun, Xichun Song, Qiang Guo, Chongjun Liang, Yuqi Sun, Wei The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review |
title | The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review |
title_full | The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review |
title_fullStr | The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review |
title_full_unstemmed | The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review |
title_short | The Role of Autophagy in Chondrocyte Metabolism and Osteoarthritis: A Comprehensive Research Review |
title_sort | role of autophagy in chondrocyte metabolism and osteoarthritis: a comprehensive research review |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6487163/ https://www.ncbi.nlm.nih.gov/pubmed/31111057 http://dx.doi.org/10.1155/2019/5171602 |
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