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Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease
Previous studies have identified a close association between diet and the prevalence of Kashin-Beck disease (KBD); however, the mechanisms via which the diet protects against KBD-associated cartilage injury has remained elusive. Recent international research studies have revealed a therapeutic role...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5844000/ https://www.ncbi.nlm.nih.gov/pubmed/29556257 http://dx.doi.org/10.3892/etm.2018.5885 |
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author | Ning, Yujie Wang, Xi Zhang, Pan Liu, Amin Qi, Xin Liu, Meidan Guo, Xiong |
author_facet | Ning, Yujie Wang, Xi Zhang, Pan Liu, Amin Qi, Xin Liu, Meidan Guo, Xiong |
author_sort | Ning, Yujie |
collection | PubMed |
description | Previous studies have identified a close association between diet and the prevalence of Kashin-Beck disease (KBD); however, the mechanisms via which the diet protects against KBD-associated cartilage injury has remained elusive. Recent international research studies have revealed a therapeutic role of dietary exosome micro (mi)RNAs in repairing chondrocyte lesions by regulating genes and proteins associated with cellular apoptosis and extracellular matrix. Vital molecules affecting bio-functions of chondrocytes, including miR-23b and protein kinase cyclic AMP-activated catalytic subunit β, were preliminarily identified to be dysregulated in cells and cartilage tissue of KBD patients. The function of dietary exosome in the repair of chondrocyte lesions in KBD is a novel topic in this field. It is worth exploring the protective role of dietary exosome-miR-23b against chondrocyte damage through the regulation of the protein kinase A (PKA) signaling pathway. The following aims are significant in future studies: i) To verify the association between exosome and cartilage damage in KBD patients; ii) to identify whether the protective mechanism of miR-23b in cartilage damage proceeds through regulating the PKA pathway; and iii) to explore the therapeutic role of dietary exosome-miR-23b in repairing chondrocyte lesions induced by environmental risk factors. These ideas may help establish the therapeutic role and mechanisms of dietary exosome-miR-23b in repairing chondrocyte lesions at the molecular, cellular and organismal level. These studies may simultaneously elucidate the disease pathogenesis and provide evidence for novel biomarkers and therapeutic methods for KBD. |
format | Online Article Text |
id | pubmed-5844000 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-58440002018-03-19 Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease Ning, Yujie Wang, Xi Zhang, Pan Liu, Amin Qi, Xin Liu, Meidan Guo, Xiong Exp Ther Med Review Previous studies have identified a close association between diet and the prevalence of Kashin-Beck disease (KBD); however, the mechanisms via which the diet protects against KBD-associated cartilage injury has remained elusive. Recent international research studies have revealed a therapeutic role of dietary exosome micro (mi)RNAs in repairing chondrocyte lesions by regulating genes and proteins associated with cellular apoptosis and extracellular matrix. Vital molecules affecting bio-functions of chondrocytes, including miR-23b and protein kinase cyclic AMP-activated catalytic subunit β, were preliminarily identified to be dysregulated in cells and cartilage tissue of KBD patients. The function of dietary exosome in the repair of chondrocyte lesions in KBD is a novel topic in this field. It is worth exploring the protective role of dietary exosome-miR-23b against chondrocyte damage through the regulation of the protein kinase A (PKA) signaling pathway. The following aims are significant in future studies: i) To verify the association between exosome and cartilage damage in KBD patients; ii) to identify whether the protective mechanism of miR-23b in cartilage damage proceeds through regulating the PKA pathway; and iii) to explore the therapeutic role of dietary exosome-miR-23b in repairing chondrocyte lesions induced by environmental risk factors. These ideas may help establish the therapeutic role and mechanisms of dietary exosome-miR-23b in repairing chondrocyte lesions at the molecular, cellular and organismal level. These studies may simultaneously elucidate the disease pathogenesis and provide evidence for novel biomarkers and therapeutic methods for KBD. D.A. Spandidos 2018-04 2018-02-22 /pmc/articles/PMC5844000/ /pubmed/29556257 http://dx.doi.org/10.3892/etm.2018.5885 Text en Copyright: © Ning et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Review Ning, Yujie Wang, Xi Zhang, Pan Liu, Amin Qi, Xin Liu, Meidan Guo, Xiong Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease |
title | Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease |
title_full | Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease |
title_fullStr | Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease |
title_full_unstemmed | Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease |
title_short | Dietary exosome-miR-23b may be a novel therapeutic measure for preventing Kashin-Beck disease |
title_sort | dietary exosome-mir-23b may be a novel therapeutic measure for preventing kashin-beck disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5844000/ https://www.ncbi.nlm.nih.gov/pubmed/29556257 http://dx.doi.org/10.3892/etm.2018.5885 |
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