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Cellular senescence of renal tubular epithelial cells in renal fibrosis
Renal fibrosis (RF) is the common pathological manifestation of virtually all chronic kidney diseases (CKD) and one of the major causes of end-stage renal disease (ESRD), but the pathogenesis of which is still unclear. Renal tubulointerstitial lesions have been identified as a key pathological hallm...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10011622/ https://www.ncbi.nlm.nih.gov/pubmed/36926022 http://dx.doi.org/10.3389/fendo.2023.1085605 |
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author | Zhang, Jun-Qing Li, Ying-Ying Zhang, Xue-Yan Tian, Zeng-Hui Liu, Cheng Wang, Shi-Tao Zhang, Fa-Rong |
author_facet | Zhang, Jun-Qing Li, Ying-Ying Zhang, Xue-Yan Tian, Zeng-Hui Liu, Cheng Wang, Shi-Tao Zhang, Fa-Rong |
author_sort | Zhang, Jun-Qing |
collection | PubMed |
description | Renal fibrosis (RF) is the common pathological manifestation of virtually all chronic kidney diseases (CKD) and one of the major causes of end-stage renal disease (ESRD), but the pathogenesis of which is still unclear. Renal tubulointerstitial lesions have been identified as a key pathological hallmark of RF pathology. Renal tubular epithelial cells are the resident cells of the tubulointerstitium and play an important role in kidney recovery versus renal fibrosis following injury. Studies in recent years have shown that senescence of renal tubular epithelial cells can accelerate the progression of renal fibrosis. Oxidative stress(OS), telomere attrition and DNA damage are the major causes of renal tubular epithelial cell senescence. Current interventions and therapeutic strategies for cellular senescence include calorie restriction and routine exercise, Klotho, senolytics, senostatics, and other related drugs. This paper provides an overview of the mechanisms and the key signaling pathways including Wnt/β-catenin/RAS, Nrf2/ARE and STAT-3/NF-κB pathway involved in renal tubular epithelial cell senescence in RF and therapies targeting renal tubular epithelial cell senescence future therapeutic potential for RF patients. These findings may offer promise for the further treatment of RF and CKD. |
format | Online Article Text |
id | pubmed-10011622 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-100116222023-03-15 Cellular senescence of renal tubular epithelial cells in renal fibrosis Zhang, Jun-Qing Li, Ying-Ying Zhang, Xue-Yan Tian, Zeng-Hui Liu, Cheng Wang, Shi-Tao Zhang, Fa-Rong Front Endocrinol (Lausanne) Endocrinology Renal fibrosis (RF) is the common pathological manifestation of virtually all chronic kidney diseases (CKD) and one of the major causes of end-stage renal disease (ESRD), but the pathogenesis of which is still unclear. Renal tubulointerstitial lesions have been identified as a key pathological hallmark of RF pathology. Renal tubular epithelial cells are the resident cells of the tubulointerstitium and play an important role in kidney recovery versus renal fibrosis following injury. Studies in recent years have shown that senescence of renal tubular epithelial cells can accelerate the progression of renal fibrosis. Oxidative stress(OS), telomere attrition and DNA damage are the major causes of renal tubular epithelial cell senescence. Current interventions and therapeutic strategies for cellular senescence include calorie restriction and routine exercise, Klotho, senolytics, senostatics, and other related drugs. This paper provides an overview of the mechanisms and the key signaling pathways including Wnt/β-catenin/RAS, Nrf2/ARE and STAT-3/NF-κB pathway involved in renal tubular epithelial cell senescence in RF and therapies targeting renal tubular epithelial cell senescence future therapeutic potential for RF patients. These findings may offer promise for the further treatment of RF and CKD. Frontiers Media S.A. 2023-02-28 /pmc/articles/PMC10011622/ /pubmed/36926022 http://dx.doi.org/10.3389/fendo.2023.1085605 Text en Copyright © 2023 Zhang, Li, Zhang, Tian, Liu, Wang and Zhang https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Endocrinology Zhang, Jun-Qing Li, Ying-Ying Zhang, Xue-Yan Tian, Zeng-Hui Liu, Cheng Wang, Shi-Tao Zhang, Fa-Rong Cellular senescence of renal tubular epithelial cells in renal fibrosis |
title | Cellular senescence of renal tubular epithelial cells in renal fibrosis |
title_full | Cellular senescence of renal tubular epithelial cells in renal fibrosis |
title_fullStr | Cellular senescence of renal tubular epithelial cells in renal fibrosis |
title_full_unstemmed | Cellular senescence of renal tubular epithelial cells in renal fibrosis |
title_short | Cellular senescence of renal tubular epithelial cells in renal fibrosis |
title_sort | cellular senescence of renal tubular epithelial cells in renal fibrosis |
topic | Endocrinology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10011622/ https://www.ncbi.nlm.nih.gov/pubmed/36926022 http://dx.doi.org/10.3389/fendo.2023.1085605 |
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