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Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy

Obesity-related glomerulopathy is an increasing cause of end-stage renal disease. Obesity has been considered a state of chronic low-grade systemic inflammation and chronic oxidative stress. Augmented inflammation in adipose and kidney tissues promotes the progression of kidney damage in obesity. Ad...

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Detalles Bibliográficos
Autores principales: Tang, Jinhua, Yan, Haidong, Zhuang, Shougang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3332212/
https://www.ncbi.nlm.nih.gov/pubmed/22567283
http://dx.doi.org/10.1155/2012/608397
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author Tang, Jinhua
Yan, Haidong
Zhuang, Shougang
author_facet Tang, Jinhua
Yan, Haidong
Zhuang, Shougang
author_sort Tang, Jinhua
collection PubMed
description Obesity-related glomerulopathy is an increasing cause of end-stage renal disease. Obesity has been considered a state of chronic low-grade systemic inflammation and chronic oxidative stress. Augmented inflammation in adipose and kidney tissues promotes the progression of kidney damage in obesity. Adipose tissue, which is accumulated in obesity, is a key endocrine organ that produces multiple biologically active molecules, including leptin, adiponectin, resistin, that affect inflammation, and subsequent deregulation of cell function in renal glomeruli that leads to pathological changes. Oxidative stress is also associated with obesity-related renal diseases and may trigger the initiation or progression of renal damage in obesity. In this paper, we focus on inflammation and oxidative stress in the progression of obesity-related glomerulopathy and possible interventions to prevent kidney injury in obesity.
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spelling pubmed-33322122012-05-07 Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy Tang, Jinhua Yan, Haidong Zhuang, Shougang Int J Nephrol Research Article Obesity-related glomerulopathy is an increasing cause of end-stage renal disease. Obesity has been considered a state of chronic low-grade systemic inflammation and chronic oxidative stress. Augmented inflammation in adipose and kidney tissues promotes the progression of kidney damage in obesity. Adipose tissue, which is accumulated in obesity, is a key endocrine organ that produces multiple biologically active molecules, including leptin, adiponectin, resistin, that affect inflammation, and subsequent deregulation of cell function in renal glomeruli that leads to pathological changes. Oxidative stress is also associated with obesity-related renal diseases and may trigger the initiation or progression of renal damage in obesity. In this paper, we focus on inflammation and oxidative stress in the progression of obesity-related glomerulopathy and possible interventions to prevent kidney injury in obesity. Hindawi Publishing Corporation 2012-04-05 /pmc/articles/PMC3332212/ /pubmed/22567283 http://dx.doi.org/10.1155/2012/608397 Text en Copyright © 2012 Jinhua Tang et al. https://creativecommons.org/licenses/by/3.0/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 Research Article
Tang, Jinhua
Yan, Haidong
Zhuang, Shougang
Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy
title Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy
title_full Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy
title_fullStr Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy
title_full_unstemmed Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy
title_short Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy
title_sort inflammation and oxidative stress in obesity-related glomerulopathy
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3332212/
https://www.ncbi.nlm.nih.gov/pubmed/22567283
http://dx.doi.org/10.1155/2012/608397
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