Mitochondrial Reactive Oxygen Species and Their Contribution in Chronic Kidney Disease Progression Through Oxidative Stress

Mitochondria are known to generate approximately 90% of cellular reactive oxygen species (ROS). The imbalance between mitochondrial reactive oxygen species (mtROS) production and removal due to overproduction of ROS and/or decreased antioxidants defense activity results in oxidative stress (OS), whi...

Full description

Saved in:
Bibliographic Details
Published in:Frontiers in physiology Vol. 12; p. 627837
Main Authors: Tirichen, Hasna, Yaigoub, Hasnaa, Xu, Weiwei, Wu, Changxin, Li, Rongshan, Li, Yafeng
Format: Journal Article
Language:English
Published: Switzerland Frontiers Media S.A 23.04.2021
Subjects:
chronic kidney disease
kidney
mitochondria
oxidative stress
Physiology
reactive oxygen species
kidney
chronic kidney disease
mitochondria
oxidative stress
reactive oxygen species
ISSN:1664-042X, 1664-042X
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Mitochondria are known to generate approximately 90% of cellular reactive oxygen species (ROS). The imbalance between mitochondrial reactive oxygen species (mtROS) production and removal due to overproduction of ROS and/or decreased antioxidants defense activity results in oxidative stress (OS), which leads to oxidative damage that affects several cellular components such as lipids, DNA, and proteins. Since the kidney is a highly energetic organ, it is more vulnerable to damage caused by OS and thus its contribution to the development and progression of chronic kidney disease (CKD). This article aims to review the contribution of mtROS and OS to CKD progression and kidney function deterioration.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
Reviewed by: Daniela Valenti, National Research Council, Italy; Claudia Lagranha, Federal University of Pernambuco, Brazil; Tingyang Zhou, The Ohio State University, United States
Edited by: Simona Martinotti, Università del Piemonte Orientale, Italy
This article was submitted to Redox Physiology, a section of the journal Frontiers in Physiology
ISSN:1664-042X
1664-042X
DOI:10.3389/fphys.2021.627837