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Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments
Renal fibrosis is the common pathway for most forms of progressive renal disease. The Unilateral Ureteral Obstruction (UUO) model is used to cause renal fibrosis, where the primary feature of UUO is tubular injury as a result of obstructed urine flow. Furthermore, experimental UUO in rodents is beli...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6523883/ https://www.ncbi.nlm.nih.gov/pubmed/30965656 http://dx.doi.org/10.3390/biom9040141 |
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author | Martínez-Klimova, Elena Aparicio-Trejo, Omar Emiliano Tapia, Edilia Pedraza-Chaverri, José |
author_facet | Martínez-Klimova, Elena Aparicio-Trejo, Omar Emiliano Tapia, Edilia Pedraza-Chaverri, José |
author_sort | Martínez-Klimova, Elena |
collection | PubMed |
description | Renal fibrosis is the common pathway for most forms of progressive renal disease. The Unilateral Ureteral Obstruction (UUO) model is used to cause renal fibrosis, where the primary feature of UUO is tubular injury as a result of obstructed urine flow. Furthermore, experimental UUO in rodents is believed to mimic human chronic obstructive nephropathy in an accelerated manner. Renal fibrosis is the common pathway for most forms of progressive renal disease. Removing the obstruction may not be sufficient to reverse fibrosis, so an accompanying treatment may be of benefit. In this review, we have done a revision on treatments shown to ameliorate fibrosis in the context of the UUO experimental model. The treatments inhibit the production of fibrotic and inflammatory proteins such as Transforming Growth Factor β1 (TGF-β(1)), Tumor Necrosis Factor α (TNF-α), collagen and fibronectin, Heat Shock Protein 47 (HSP47), suppress the proliferation of fibroblasts, prevent epithelial-to-mesenchymal transition, reduce oxidative stress, inhibit the action of the Nuclear Factor κB (NF-κB), reduce the phosphorylation of mothers against decapentaplegic homolog (SMAD) family members 2 and 3 (Smad2/3) or Mitogen-Activated Protein Kinases (MAPKs), inhibit the activation of the renin-angiotensin system. Summaries of the UUO experimental methods and alterations observed in the UUO experiments are included. |
format | Online Article Text |
id | pubmed-6523883 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-65238832019-06-03 Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments Martínez-Klimova, Elena Aparicio-Trejo, Omar Emiliano Tapia, Edilia Pedraza-Chaverri, José Biomolecules Review Renal fibrosis is the common pathway for most forms of progressive renal disease. The Unilateral Ureteral Obstruction (UUO) model is used to cause renal fibrosis, where the primary feature of UUO is tubular injury as a result of obstructed urine flow. Furthermore, experimental UUO in rodents is believed to mimic human chronic obstructive nephropathy in an accelerated manner. Renal fibrosis is the common pathway for most forms of progressive renal disease. Removing the obstruction may not be sufficient to reverse fibrosis, so an accompanying treatment may be of benefit. In this review, we have done a revision on treatments shown to ameliorate fibrosis in the context of the UUO experimental model. The treatments inhibit the production of fibrotic and inflammatory proteins such as Transforming Growth Factor β1 (TGF-β(1)), Tumor Necrosis Factor α (TNF-α), collagen and fibronectin, Heat Shock Protein 47 (HSP47), suppress the proliferation of fibroblasts, prevent epithelial-to-mesenchymal transition, reduce oxidative stress, inhibit the action of the Nuclear Factor κB (NF-κB), reduce the phosphorylation of mothers against decapentaplegic homolog (SMAD) family members 2 and 3 (Smad2/3) or Mitogen-Activated Protein Kinases (MAPKs), inhibit the activation of the renin-angiotensin system. Summaries of the UUO experimental methods and alterations observed in the UUO experiments are included. MDPI 2019-04-08 /pmc/articles/PMC6523883/ /pubmed/30965656 http://dx.doi.org/10.3390/biom9040141 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Martínez-Klimova, Elena Aparicio-Trejo, Omar Emiliano Tapia, Edilia Pedraza-Chaverri, José Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments |
title | Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments |
title_full | Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments |
title_fullStr | Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments |
title_full_unstemmed | Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments |
title_short | Unilateral Ureteral Obstruction as a Model to Investigate Fibrosis-Attenuating Treatments |
title_sort | unilateral ureteral obstruction as a model to investigate fibrosis-attenuating treatments |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6523883/ https://www.ncbi.nlm.nih.gov/pubmed/30965656 http://dx.doi.org/10.3390/biom9040141 |
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