NADPH oxidase inhibitor development for diabetic nephropathy through water tank model

Hye Eun Lee; Seunghwan Shim; Yongseok Choi; Yun Soo Bae

doi:10.23876/j.krcp.21.269

NADPH oxidase inhibitor development for diabetic nephropathy through water tank model

Hye Eun Lee, Seunghwan Shim, Yongseok Choi, Yun Soo Bae

Department of Life Science

Research output: Contribution to journal › Review article › peer-review

7 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	S89-S98
Journal	Kidney Research and Clinical Practice
Volume	41
DOIs	https://doi.org/10.23876/j.krcp.21.269
State	Published - 1 Sep 2022

Bibliographical note

Funding 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.

Publisher Copyright:
© 2022 by The Korean Society of Nephrology.

Keywords

Diabetic nephropathies
NADPH oxidases
Nox inhibitor
Oxidative stress
Reactive oxygen species

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10.23876/j.krcp.21.269

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title = "NADPH oxidase inhibitor development for diabetic nephropathy through water tank model",

abstract = "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.",

keywords = "Diabetic nephropathies, NADPH oxidases, Nox inhibitor, Oxidative stress, Reactive oxygen species",

author = "Lee, {Hye Eun} and Seunghwan Shim and Yongseok Choi and Bae, {Yun Soo}",

note = "Funding 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. Publisher Copyright: {\textcopyright} 2022 by The Korean Society of Nephrology.",

year = "2022",

month = sep,

day = "1",

doi = "10.23876/j.krcp.21.269",

language = "English",

volume = "41",

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TY - JOUR

T1 - NADPH oxidase inhibitor development for diabetic nephropathy through water tank model

AU - Lee, Hye Eun

AU - Shim, Seunghwan

AU - Choi, Yongseok

AU - Bae, Yun Soo

N1 - Funding 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. Publisher Copyright: © 2022 by The Korean Society of Nephrology.

PY - 2022/9/1

Y1 - 2022/9/1

N2 - 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.

AB - 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.

KW - Diabetic nephropathies

KW - NADPH oxidases

KW - Nox inhibitor

KW - Oxidative stress

KW - Reactive oxygen species

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U2 - 10.23876/j.krcp.21.269

DO - 10.23876/j.krcp.21.269

M3 - Review article

AN - SCOPUS:85139471498

SN - 2211-9132

VL - 41

SP - S89-S98

JO - Kidney Research and Clinical Practice

JF - Kidney Research and Clinical Practice

ER -

NADPH oxidase inhibitor development for diabetic nephropathy through water tank model

Abstract

Bibliographical note

Keywords

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