Edaravone for Potential Mitigation of Oxidative Stress and Inflammation in Kidney Disease
- 1Department of Pharmaceutical Sciences, UNT System College of Pharmacy and Health Professions, UNT Health Fort Worth, Fort Worth, TX 76107, USA
Abstract
Edaravone (EDA) is a synthetic free-radical scavenger FDA-approved for amyotrophic lateral sclerosis (ALS) treatment in the United States and is used clinically for treatment of acute ischemic stroke in Japan and other countries. While its antioxidant activity has been the primary focus of investigation in the mitigation of oxidative-stress-related injury, EDA exhibits anti-inflammatory, anti-fibrotic, anti-apoptotic, and anti-necrotic effects in animal models. These properties make it a potentially attractive therapeutic agent for kidney disease, where oxidative stress and inflammation contribute to renal cell injury, mitochondrial dysfunction, and progression of disease. In this review, we cover the underlying mechanisms of oxidative stress and inflammation in renal injury, and pharmacological and free-radical-scavenging mechanisms of EDA. Preclinical evidence in several kidney diseases, including ischemic/reperfusion injury, nephrotoxin-induced disease, and diabetic kidney disease, has been used to assess EDA for efficacy. In addition, we explore the modulatory roles of key signaling pathways, such as Nrf2 and NF-κB, in protective effects of EDA against oxidative stress, inflammation, mitochondrial dysfunction, apoptosis, necrosis, and fibrosis. Finally, we highlight the potential of EDA as a therapy in future clinical applications for various kidney diseases such as acute kidney injury (AKI) and chronic kidney disease (CKD). It should also be emphasized that as EDA’s renal efficacy evidence described in this review is largely limited to animal studies, robust human clinical data are lacking. Therefore, additional clinical studies are still needed to fully elucidate the efficacy, safety, and benefits of EDA for prevention and treatment of human kidney disease.
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BibTeX
@article{mohamed2026edaravone,
title = {{Edaravone for Potential Mitigation of Oxidative Stress and Inflammation in Kidney Disease}},
author = {Yasmeen K. Mohamed and Liang-Jun Yan},
journal = {Biomolecules},
year = {2026},
month = oct,
doi = {10.3390/biom16101490},
url = {https://www.mdpi.com/2218-273X/16/10/1490},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Edaravone for Potential Mitigation of Oxidative Stress and Inflammation in Kidney Disease
AU - Yasmeen K. Mohamed
AU - Liang-Jun Yan
PY - 2026
DA - 2026/10/13
JO - Biomolecules
DO - 10.3390/biom16101490
UR - https://www.mdpi.com/2218-273X/16/10/1490
AB - Edaravone (EDA) is a synthetic free-radical scavenger FDA-approved for amyotrophic lateral sclerosis (ALS) treatment in the United States and is used clinically for treatment of acute ischemic stroke in Japan and other countries. While its antioxidant activity has been the primary focus of investigation in the mitigation of oxidative-stress-related injury, EDA exhibits anti-inflammatory, anti-fibrotic, anti-apoptotic, and anti-necrotic effects in animal models. These properties make it a potentially attractive therapeutic agent for kidney disease, where oxidative stress and inflammation contribute to renal cell injury, mitochondrial dysfunction, and progression of disease. In this review, we cover the underlying mechanisms of oxidative stress and inflammation in renal injury, and pharmacological and free-radical-scavenging mechanisms of EDA. Preclinical evidence in several kidney diseases, including ischemic/reperfusion injury, nephrotoxin-induced disease, and diabetic kidney disease, has been used to assess EDA for efficacy. In addition, we explore the modulatory roles of key signaling pathways, such as Nrf2 and NF-κB, in protective effects of EDA against oxidative stress, inflammation, mitochondrial dysfunction, apoptosis, necrosis, and fibrosis. Finally, we highlight the potential of EDA as a therapy in future clinical applications for various kidney diseases such as acute kidney injury (AKI) and chronic kidney disease (CKD). It should also be emphasized that as EDA’s renal efficacy evidence described in this review is largely limited to animal studies, robust human clinical data are lacking. Therefore, additional clinical studies are still needed to fully elucidate the efficacy, safety, and benefits of EDA for prevention and treatment of human kidney disease.
SN - 2218-273X
ER -