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Metabolic reprogramming heterogeneity in chronic kidney disease
Fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of chronic kidney disease (CKD). Myofibroblasts, which are the cells responsible for ECM production, are activated by cross talk with injured proximal tubule and immune cells. Emerging evidence suggests that alte...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10315765/ https://www.ncbi.nlm.nih.gov/pubmed/36723270 http://dx.doi.org/10.1002/2211-5463.13568 |
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author | Miguel, Verónica Kramann, Rafael |
author_facet | Miguel, Verónica Kramann, Rafael |
author_sort | Miguel, Verónica |
collection | PubMed |
description | Fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of chronic kidney disease (CKD). Myofibroblasts, which are the cells responsible for ECM production, are activated by cross talk with injured proximal tubule and immune cells. Emerging evidence suggests that alterations in metabolism are not only a feature of but also play an influential role in the pathogenesis of renal fibrosis. The application of omics technologies to cell‐tracing animal models and follow‐up functional data suggest that cell‐type‐specific metabolic shifts have particular roles in the fibrogenic response. In this review, we cover the main metabolic reprogramming outcomes in renal fibrosis and provide a future perspective on the field of renal fibrometabolism. |
format | Online Article Text |
id | pubmed-10315765 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-103157652023-07-04 Metabolic reprogramming heterogeneity in chronic kidney disease Miguel, Verónica Kramann, Rafael FEBS Open Bio Reviews Fibrosis driven by excessive accumulation of extracellular matrix (ECM) is the hallmark of chronic kidney disease (CKD). Myofibroblasts, which are the cells responsible for ECM production, are activated by cross talk with injured proximal tubule and immune cells. Emerging evidence suggests that alterations in metabolism are not only a feature of but also play an influential role in the pathogenesis of renal fibrosis. The application of omics technologies to cell‐tracing animal models and follow‐up functional data suggest that cell‐type‐specific metabolic shifts have particular roles in the fibrogenic response. In this review, we cover the main metabolic reprogramming outcomes in renal fibrosis and provide a future perspective on the field of renal fibrometabolism. John Wiley and Sons Inc. 2023-02-14 /pmc/articles/PMC10315765/ /pubmed/36723270 http://dx.doi.org/10.1002/2211-5463.13568 Text en © 2023 The Authors. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Reviews Miguel, Verónica Kramann, Rafael Metabolic reprogramming heterogeneity in chronic kidney disease |
title | Metabolic reprogramming heterogeneity in chronic kidney disease |
title_full | Metabolic reprogramming heterogeneity in chronic kidney disease |
title_fullStr | Metabolic reprogramming heterogeneity in chronic kidney disease |
title_full_unstemmed | Metabolic reprogramming heterogeneity in chronic kidney disease |
title_short | Metabolic reprogramming heterogeneity in chronic kidney disease |
title_sort | metabolic reprogramming heterogeneity in chronic kidney disease |
topic | Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10315765/ https://www.ncbi.nlm.nih.gov/pubmed/36723270 http://dx.doi.org/10.1002/2211-5463.13568 |
work_keys_str_mv | AT miguelveronica metabolicreprogrammingheterogeneityinchronickidneydisease AT kramannrafael metabolicreprogrammingheterogeneityinchronickidneydisease |