Hormonal and Redox Regulation in Cancer, Metabolic Dysfunction, and Neurodegenerative Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 980

Special Issue Editor


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Guest Editor
Department of Pathology, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea
Interests: cancer; redox; endocrinology; herbal medicine; pathology; cancer stem cell; cancer reprogramming; miRNA; alternative splicing factor; drug resistance; drug development; drug delivery system
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Special Issue Information

Dear Colleagues,

Hormonal signaling and redox homeostasis form an essential regulatory axis in cancer, metabolic dysfunction, and neurodegenerative diseases. Hormones such as melatonin, estrogen, insulin, and glucocorticoids act not only as systemic messengers but also as intracellular antioxidants and transcriptional modulators, shaping cellular decisions involving survival, apoptosis, and differentiation.

These molecules influence oxidative stress, mitochondrial integrity, and epigenetic reprogramming through pathways such as Nrf2/Keap1, PI3K/AKT/mTOR, AMPK/SIRT1, and NF-κB, ultimately regulating inflammation, metabolic rewriting, ferroptosis, and immune response. Moreover, redox-sensitive regulation of noncoding RNAs (miRNA, IncRNA) provides an additional epigenetic layer linking endocrine activity to oxidative adaption.

This Special issue invites multidisciplinary research exploring the molecular, pharmacological, redox-biological, and translational roles of hormones in human disease. Submissions may include experimental studies, clinical–translational research, or computational modeling. Mechanistic insights, omics-driven discoveries, natural-product-based therapeutics, redox-targeting strategies, and biomarker development are especially encouraged.

Topics of interest (include but not limited to)

  • Hormonal control of redox signaling in cancer, metabolic disorders, and neurodegeneration;
  • Melatonin as a redox modulator: mitochondrial regulation and epigenetic remodeling;
  • Crosstalk between insulin/IGF and ROS in metabolic reprogramming;
  • Redox-dependent regulation of apoptosis, autophagy, and ferroptosis in endocrine-related diseases;
  • Circadian rhythm, endocrine fluctuations, and oxidative homeostasis;
  • Translational and pharmacological strategies targeting hormone–redox interactions;
  • Computational and pharmacoinformatic modeling of hormone-associated redox modulators;
  • Synergistic actions of natural compounds with hormonal pathways in oxidative-stress-related disorders.

Dr. Moon Nyeo Park
Guest Editor

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Keywords

  • hormonal regulation
  • redox signaling
  • antioxidant hormones
  • melatonin
  • oxidative stress
  • mitochondria
  • epigenetics
  • noncoding RNA
  • metabolic reprogramming
  • ferroptosis
  • inflammation
  • SIRT1/AMPK
  • Nrf2/Keap1
  • redox therapeutics
  • translational pharmacology
  • natural compounds
 

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Published Papers (1 paper)

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Review

43 pages, 1431 KB  
Review
Therapy as a State-Generator: Dynamic Phenotypic Landscapes and Adaptive Stress Circuits in Chemotherapy Resistance of Breast Cancer
by Moon Nyeo Park
Antioxidants 2026, 15(4), 459; https://doi.org/10.3390/antiox15040459 - 8 Apr 2026
Viewed by 685
Abstract
Chemotherapy resistance remains a major obstacle to durable cancer control, yet its underlying mechanisms cannot be fully explained by genetic mutations alone. Increasing evidence suggests that therapeutic stress induces dynamic adaptive programs that reshape tumor phenotypic landscapes. Here, we propose a systems-level framework [...] Read more.
Chemotherapy resistance remains a major obstacle to durable cancer control, yet its underlying mechanisms cannot be fully explained by genetic mutations alone. Increasing evidence suggests that therapeutic stress induces dynamic adaptive programs that reshape tumor phenotypic landscapes. Here, we propose a systems-level framework in which chemotherapy resistance emerges from the stabilization of interconnected stress-response circuits integrating redox signaling, metabolic reprogramming, and transcriptional plasticity. In this model, cytotoxic therapies function as state-generating perturbations that elevate oxidative stress and activate adaptive buffering systems, including NADPH-dependent redox homeostasis, replication stress tolerance, and integrated stress response (ISR)-mediated translational reprogramming. These adaptive modules collectively expand the accessibility of therapy-tolerant phenotypic states within tumor cell populations. Importantly, these circuits coordinate mitochondrial redox homeostasis, metabolic NADPH regeneration, and epigenetic–transcriptional plasticity to sustain cellular survival under persistent oxidative pressure. Such adaptive redox networks not only stabilize stress-tolerant phenotypes but also create vulnerabilities that can be therapeutically exploited. From a translational perspective, this framework suggests that effective strategies to overcome chemotherapy resistance should move beyond single-target inhibition and instead focus on circuit-guided therapeutic interventions that simultaneously destabilize redox buffering systems, constrain phenotypic plasticity, and disrupt metabolic stress adaptation. By conceptualizing therapy resistance as a dynamic redox-regulated state-space phenomenon, this model provides a mechanistic foundation for the development of evolution-aware and plasticity-constraining therapeutic strategies. Targeting the coordinated redox–metabolic–translational circuits that maintain tumor adaptability may therefore represent a promising direction for next-generation redox therapeutics in cancer. Full article
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