Thiol–Redox-Mediated Cell Death in Human Disease: Pathogenic Mechanisms and Therapeutic Intervention
A Special Issue of Antioxidants (ISSN 2076-3921) belonging to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: 28 February 2027 | Viewed by 2
Editors
Interests: thiol; antioxidants; thioredoxin; glutaredoxin; selenium; molecular docking; pharmacology/toxicology; drug-induced liver injury; metabolic-associated fatty liver disease; diabetes; psoriasis; inflammatory bowel disease; systems metabolic engineering
Special Issues, Collections and Topics in MDPI journals
Interests: selenium; antioxidants; thioredoxin reductase; glutathione peroxidase; programmed cell death; ferroptosis; disulfidptosis
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Cellular thiol–disulfide imbalance is a common hallmark of multiple programmed cell death pathways, including apoptosis, ferroptosis, pyroptosis, and the recently identified disulfidptosis. Consequently, this imbalance contributes to the pathogenesis of various human disorders, ranging from cancer, neurodegenerative disorders, and diabetes to metabolic-associated fatty liver disease, psoriasis, infections, and inflammatory diseases. Intracellular thiol homeostasis is primarily maintained by two major thiol-dependent systems: the thioredoxin (Trx) system and the glutaredoxin (Grx) system. The Trx system comprises NADPH, the selenoprotein thioredoxin reductase, thioredoxin, coupled with thioredoxin-dependent peroxidases (peroxiredoxins), and Trx activity is negatively regulated by endogenous TXNIP. In parallel, the Grx system consists of NADPH, glutathione, glutaredoxin, and is coupled with another critical selenoprotein—glutathione peroxidase. These two thiol–redox systems function synergistically and compensatively, forming an integrated antioxidant network. Disruption of this thiol–redox network serves as a pivotal regulatory node in programmed cell death and is closely linked to disease development. Accordingly, therapeutic strategies aimed at modulating this redox network represent promising interventions for disease prevention and treatment. Notably, a variety of sulfur- or selenium-containing compounds, along with natural antioxidants, have been shown to modulate the activities of the Trx and Grx systems, highlighting their potential as drug candidates against these disorders.
This Special Issue aims to address our mechanistic understanding and therapeutic exploitation of these thiol redox systems in human diseases. Original research articles, review articles, and short communications are welcome in this Special Issue.
Prof. Dr. Jun Lu
Dr. Jianqiang Xu
Guest Editors
Manuscript Submission Information
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Keywords
- thiol
- redox regulation
- thioredoxin
- glutaredoxin
- selenoprotein
- pathogenesis
- therapy
- antioxidant
- inflammation
- metabolism
- cell death
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