期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 172, 期 -, 页码 65-81出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2021.05.034
关键词
Unilateral ureteral obstruction (UUO); Angiotensin II (Ang II); NADPH oxidases (NOXs); Reactive oxygen species (ROS); Redox signaling; Redox-sensitive proteins; Oxidative stress; Mitochondria; Mitochondrial ROS (mtROS)
资金
- CONACyT, Mexico [CVU 818062, CVU 637627]
- Direccion General de Asuntos Academicos (DGAPA) , UNAM
In the UUO model, overproduction of ROS leads to alterations in signaling pathways, promoting inflammation, oxidative stress, and apoptosis, contributing to fibrosis development. Impairment of mitochondrial metabolism is also involved in this process.
Unilateral ureteral obstruction (UUO) is an experimental rodent model that mimics renal fibrosis associated with obstructive nephropathy in an accelerated manner. After UUO, the activation of the renin-angiotensin system (RAS), nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) and mitochondrial dysfunction lead to reactive oxygen species (ROS) overproduction in the kidney. ROS are secondary messengers able to induce post-translational modifications (PTMs) in redox-sensitive proteins, which activate or deactivate signaling pathways. Therefore, in UUO, it has been proposed that ROS overproduction causes changes in said pathways promoting inflammation, oxidative stress, and apoptosis that contribute to fibrosis development. Furthermore, mitochondrial metabolism impairment has been associated with UUO, contributing to renal damage in this model. Although ROS production and oxidative stress have been studied in UUO, the development of renal fibrosis associated with redox signaling pathways has not been addressed. This review focuses on the current information about the activation and deactivation of signaling pathways sensitive to a redox state and their effect on mitochondrial metabolism in the fibrosis development in the UUO model.
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