Oxidative stress can cause generation of uncontrolled reactive oxygen species (ROS) and lead to cytotoxic damage to cells and tissues. Recently, it has been shown that transient ROS generation can serve as a secondary messenger in receptor-mediated cell signaling. Although excessive levels of ROS are harmful, moderated levels of ROS are essential for normal physiological function. Therefore, regulating cellular ROS levels should be an important concept for development of novel therapeutics for treating diseases. The overexpression and hyperactivation of NADPH oxidase (Nox) can induce high levels of ROS, which are strongly associated with diabetic nephropathy. This review discusses the theoretical basis for development of the Nox inhibitor as a regulator of ROS homeostasis to provide emerging therapeutic opportunities for diabetic nephropathy.
Bibliographical noteFunding Information:
A9D8062955 to YSB) and Bio-SPC (2018M3A9G1075771 to YSB) funded by the National Research Foundation of Korea (NRF) and Ministry of Science and ICT, and by a grant from the Korea Health Technology R&D Project (HI21C0293 to HEL) through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare.
© 2022 by The Korean Society of Nephrology.
- Diabetic nephropathies
- NADPH oxidases
- Nox inhibitor
- Oxidative stress
- Reactive oxygen species
ASJC Scopus subject areas