Oxidative stress and the role of redox signalling in chronic kidney disease

被引:63
|
作者
Kishi, Seiji [1 ]
Nagasu, Hajime [1 ]
Kidokoro, Kengo [1 ]
Kashihara, Naoki [1 ]
机构
[1] Kawasaki Med Sch, Dept Nephrol & Hypertens, Kurashiki, Okayama, Japan
关键词
NITRIC-OXIDE SYNTHASE; NF-KAPPA-B; ENDOPLASMIC-RETICULUM STRESS; IMPROVES ENDOTHELIAL FUNCTION; TRANSCRIPTION FACTOR NRF2; HYPOXIA-INDUCIBLE FACTOR; MITOCHONDRIAL-DNA; ISCHEMIA-REPERFUSION; BARDOXOLONE METHYL; HYDROGEN-PEROXIDE;
D O I
10.1038/s41581-023-00775-0
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Chronic kidney disease (CKD) is a major public health concern, underscoring a need to identify pathogenic mechanisms and potential therapeutic targets. Reactive oxygen species (ROS) are derivatives of oxygen molecules that are generated during aerobic metabolism and are involved in a variety of cellular functions that are governed by redox conditions. Low levels of ROS are required for diverse processes, including intracellular signal transduction, metabolism, immune and hypoxic responses, and transcriptional regulation. However, excess ROS can be pathological, and contribute to the development and progression of chronic diseases. Despite evidence linking elevated levels of ROS to CKD development and progression, the use of low-molecular-weight antioxidants to remove ROS has not been successful in preventing or slowing disease progression. More recent advances have enabled evaluation of the molecular interactions between specific ROS and their targets in redox signalling pathways. Such studies may pave the way for the development of sophisticated treatments that allow the selective control of specific ROS-mediated signalling pathways.
引用
收藏
页码:101 / 119
页数:19
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