Redox regulation: mechanisms, biology and therapeutic targets in diseases

被引:0
|
作者
Li, Bowen [1 ,2 ,3 ]
Ming, Hui [1 ,2 ,3 ]
Qin, Siyuan [1 ,2 ,3 ,4 ]
Nice, Edouard C. [5 ]
Dong, Jingsi [6 ,7 ]
Du, Zhongyan [8 ,9 ]
Huang, Canhua [1 ,2 ,3 ,4 ]
机构
[1] Sichuan Univ, Inst Oxidat Stress Med, Canc Ctr, Dept Biotherapy, Chengdu, Peoples R China
[2] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu, Peoples R China
[3] Sichuan Univ, West China Sch Basic Med Sci & Forens Med, Chengdu, Peoples R China
[4] Frontiers Med Ctr, Tianfu Jincheng Lab, Chengdu, Peoples R China
[5] Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic, Australia
[6] Sichuan Univ, West China Hosp, Dept Thorac Surg, Chengdu, Sichuan, Peoples R China
[7] Sichuan Univ, West China Hosp, Lung Canc Inst, Lung Canc Ctr, Chengdu, Sichuan, Peoples R China
[8] Zhejiang Chinese Med Univ, Sch Basic Med Sci, Hangzhou, Peoples R China
[9] Key Lab Blood Stasis Toxin Syndrome Zhejiang Prov, Hangzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
ACTIVATED PROTEIN-KINASE; OXIDATIVE DNA-DAMAGE; GENE-EXPRESSION; POSTTRANSLATIONAL MODIFICATION; TRANSCRIPTION FACTORS; HISTONE DEACETYLASES; COLORECTAL-CANCER; N-ACETYLCYSTEINE; S-NITROSYLATION; TUMOR-CELLS;
D O I
10.1038/s41392-024-02095-6
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Redox signaling acts as a critical mediator in the dynamic interactions between organisms and their external environment, profoundly influencing both the onset and progression of various diseases. Under physiological conditions, oxidative free radicals generated by the mitochondrial oxidative respiratory chain, endoplasmic reticulum, and NADPH oxidases can be effectively neutralized by NRF2-mediated antioxidant responses. These responses elevate the synthesis of superoxide dismutase (SOD), catalase, as well as key molecules like nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione (GSH), thereby maintaining cellular redox homeostasis. Disruption of this finely tuned equilibrium is closely linked to the pathogenesis of a wide range of diseases. Recent advances have broadened our understanding of the molecular mechanisms underpinning this dysregulation, highlighting the pivotal roles of genomic instability, epigenetic modifications, protein degradation, and metabolic reprogramming. These findings provide a foundation for exploring redox regulation as a mechanistic basis for improving therapeutic strategies. While antioxidant-based therapies have shown early promise in conditions where oxidative stress plays a primary pathological role, their efficacy in diseases characterized by complex, multifactorial etiologies remains controversial. A deeper, context-specific understanding of redox signaling, particularly the roles of redox-sensitive proteins, is critical for designing targeted therapies aimed at re-establishing redox balance. Emerging small molecule inhibitors that target specific cysteine residues in redox-sensitive proteins have demonstrated promising preclinical outcomes, setting the stage for forthcoming clinical trials. In this review, we summarize our current understanding of the intricate relationship between oxidative stress and disease pathogenesis and also discuss how these insights can be leveraged to optimize therapeutic strategies in clinical practice.
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页数:29
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