Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Abstract The glutathione (GSH) system is considered to be one of the most powerful endogenous antioxidant systems in the cardiovascular system due to its key contribution to detoxifying xenobiotics and scavenging overreactive oxygen species (ROS). Numerous investigations have suggested that disrupti...

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Main Authors: Mingyue Tan, Yunfei Yin, Xiao Ma, Jun Zhang, Wanqian Pan, Minghao Tan, Yongjian Zhao, Tianke Yang, Tingbo Jiang, Hongxia Li
Format: Article
Language:English
Published: Nature Publishing Group 2023-02-01
Series:Cell Death and Disease
Online Access:https://doi.org/10.1038/s41419-023-05645-y
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author Mingyue Tan
Yunfei Yin
Xiao Ma
Jun Zhang
Wanqian Pan
Minghao Tan
Yongjian Zhao
Tianke Yang
Tingbo Jiang
Hongxia Li
author_facet Mingyue Tan
Yunfei Yin
Xiao Ma
Jun Zhang
Wanqian Pan
Minghao Tan
Yongjian Zhao
Tianke Yang
Tingbo Jiang
Hongxia Li
author_sort Mingyue Tan
collection DOAJ
description Abstract The glutathione (GSH) system is considered to be one of the most powerful endogenous antioxidant systems in the cardiovascular system due to its key contribution to detoxifying xenobiotics and scavenging overreactive oxygen species (ROS). Numerous investigations have suggested that disruption of the GSH system is a critical element in the pathogenesis of myocardial injury. Meanwhile, a newly proposed type of cell death, ferroptosis, has been demonstrated to be closely related to the GSH system, which affects the process and outcome of myocardial injury. Moreover, in facing various pathological challenges, the mammalian heart, which possesses high levels of mitochondria and weak antioxidant capacity, is susceptible to oxidant production and oxidative damage. Therefore, targeted enhancement of the GSH system along with prevention of ferroptosis in the myocardium is a promising therapeutic strategy. In this review, we first systematically describe the physiological functions and anabolism of the GSH system, as well as its effects on cardiac injury. Then, we discuss the relationship between the GSH system and ferroptosis in myocardial injury. Moreover, a comprehensive summary of the activation strategies of the GSH system is presented, where we mainly identify several promising herbal monomers, which may provide valuable guidelines for the exploration of new therapeutic approaches.
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spelling doaj.art-671fef317b064cc2adc9d686c0d1b90c2023-03-22T12:32:51ZengNature Publishing GroupCell Death and Disease2041-48892023-02-0114211910.1038/s41419-023-05645-yGlutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosisMingyue Tan0Yunfei Yin1Xiao Ma2Jun Zhang3Wanqian Pan4Minghao Tan5Yongjian Zhao6Tianke Yang7Tingbo Jiang8Hongxia Li9Department of Cardiology, The First Affiliated Hospital of Soochow UniversityDepartment of Cardiology, The First Affiliated Hospital of Soochow UniversityDepartment of Cardiology, The First Affiliated Hospital of Soochow UniversityDepartment of Cardiology, The First Affiliated Hospital of Soochow UniversityDepartment of Cardiology, The First Affiliated Hospital of Soochow UniversityDepartment of Nursing, Tianfu College, Southwestern University of Finance and EconomicsDepartment of Cardiology, The First Affiliated Hospital of Soochow UniversityDepartment of Ophthalmology, Eye Institute, Eye & ENT Hospital, Fudan UniversityDepartment of Cardiology, The First Affiliated Hospital of Soochow UniversityDepartment of Cardiology, The First Affiliated Hospital of Soochow UniversityAbstract The glutathione (GSH) system is considered to be one of the most powerful endogenous antioxidant systems in the cardiovascular system due to its key contribution to detoxifying xenobiotics and scavenging overreactive oxygen species (ROS). Numerous investigations have suggested that disruption of the GSH system is a critical element in the pathogenesis of myocardial injury. Meanwhile, a newly proposed type of cell death, ferroptosis, has been demonstrated to be closely related to the GSH system, which affects the process and outcome of myocardial injury. Moreover, in facing various pathological challenges, the mammalian heart, which possesses high levels of mitochondria and weak antioxidant capacity, is susceptible to oxidant production and oxidative damage. Therefore, targeted enhancement of the GSH system along with prevention of ferroptosis in the myocardium is a promising therapeutic strategy. In this review, we first systematically describe the physiological functions and anabolism of the GSH system, as well as its effects on cardiac injury. Then, we discuss the relationship between the GSH system and ferroptosis in myocardial injury. Moreover, a comprehensive summary of the activation strategies of the GSH system is presented, where we mainly identify several promising herbal monomers, which may provide valuable guidelines for the exploration of new therapeutic approaches.https://doi.org/10.1038/s41419-023-05645-y
spellingShingle Mingyue Tan
Yunfei Yin
Xiao Ma
Jun Zhang
Wanqian Pan
Minghao Tan
Yongjian Zhao
Tianke Yang
Tingbo Jiang
Hongxia Li
Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis
Cell Death and Disease
title Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis
title_full Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis
title_fullStr Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis
title_full_unstemmed Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis
title_short Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis
title_sort glutathione system enhancement for cardiac protection pharmacological options against oxidative stress and ferroptosis
url https://doi.org/10.1038/s41419-023-05645-y
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