Advances in Oxidative Stress, Mitochondrial Dysfunction and Antioxidant Therapies in Endocrine and Metabolic Disorders

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 560

Editors


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Guest Editor
Department of Physiopathology, Faculty of Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy, 3-4 Victor Babes Street, 400012 Cluj-Napoca, Romania
Interests: bariatric surgery; obesity; gut microbiota; micronutrient deficiency; probiotics
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Guest Editor Assistant
Department of Physiopathology, Faculty of Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy, 3-4 Victor Babes Street, 400012 Cluj-Napoca, Romania
Interests: diabetes; PCOS; antioxidant; inflammation; phytochemical; oxidative stress; NLRP3 inflammasome

Special Issue Information

Dear Colleagues,

Oxidative stress and mitochondrial dysfunction are increasingly being recognized as key contributors to the pathogenesis and progression of endocrine and metabolic disorders. Excessive production of reactive oxygen species (ROS), impaired antioxidant defense mechanisms, and alterations in mitochondrial bioenergetics have been implicated in a wide range of conditions, including diabetes mellitus, obesity, metabolic syndrome, thyroid diseases, adrenal disorders, osteoporosis, and reproductive endocrinopathies. These processes contribute to chronic inflammation, insulin resistance, cellular dysfunction, and tissue damage, ultimately affecting disease onset, progression, and clinical outcomes.

Recent advances in molecular biology, metabolomics, and redox medicine have improved our understanding of the complex interactions between oxidative stress, mitochondrial homeostasis, and endocrine regulation. Moreover, growing evidence has highlighted the therapeutic potential of antioxidants, mitochondrial-targeted interventions, and lifestyle-based strategies in preventing or mitigating disease-related complications.

This Special Issue aims to provide a comprehensive overview of current research on the role of oxidative stress and mitochondrial dysfunction in endocrine and metabolic diseases. We welcome the submission of original research articles, reviews, systematic reviews, and meta-analyses that address molecular mechanisms, biomarkers, novel antioxidant therapies, mitochondrial-targeted treatments, redox signaling pathways, and translational approaches with potential clinical applications. By bringing together multidisciplinary perspectives, this Special Issue seeks to advance knowledge and foster innovative therapeutic strategies in endocrine and metabolic medicine.

Prof. Dr. Adriana Florinela Càtoi
Guest Editor

Dr. Lia Oxana Usatiuc
Guest Editor Assistant

Manuscript Submission Information

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Keywords

  • reactive oxygen species (ROS)
  • mitochondrial bioenergetics
  • insulin resistance
  • antioxidant therapy

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Published Papers (1 paper)

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Research

18 pages, 2986 KB  
Article
AGEs–RAGE Axis and Mitochondrial-Derived Peptides in Advanced Chronic Kidney Disease: Interconnected Pathways Beyond Inflammation and Nutrition
by Mohamed E. Suliman, Awahan Rahman, Abdul-Rashid Qureshi, Peter Barany, Peter Stenvinkel, Karolina Kublickiene and Bengt Lindholm
Antioxidants 2026, 15(8), 956; https://doi.org/10.3390/antiox15080956 - 30 Jul 2026
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Abstract
Background. Chronic kidney disease [CKD] is characterized by increased glycoxidative stress, inflammation, and mitochondrial dysfunction. Advanced glycation end-products [AGEs] and their receptor [RAGE] mediate glycoxidative stress, whereas mitochondrial-derived peptides [MDPs], including humanin [HN], MOTS-c, and humanin-like 1 [HN-L1], regulate mitochondrial stress responses. We [...] Read more.
Background. Chronic kidney disease [CKD] is characterized by increased glycoxidative stress, inflammation, and mitochondrial dysfunction. Advanced glycation end-products [AGEs] and their receptor [RAGE] mediate glycoxidative stress, whereas mitochondrial-derived peptides [MDPs], including humanin [HN], MOTS-c, and humanin-like 1 [HN-L1], regulate mitochondrial stress responses. We investigated links between AGE–RAGE activation and mitochondrial signaling in CKD. Methods. Serum AGEs, soluble RAGE isoforms, and MDPs were measured by ELISA in 160 adults with kidney failure undergoing living-donor kidney transplantation and in 80 controls, Results. CKD patients showed higher AGEs and esRAGE, lower AGEs/sRAGE ratios, and reduced MDPs. AGEs correlated positively with sRAGE, cRAGE, and HN, while MOTS-c was inversely associated with AGEs and the AGEs/sRAGE ratio. In multivariable analyses, HN remained independently associated with AGEs, sRAGE, and the AGEs/sRAGE ratio, whereas MOTS-c showed an inverse association with the AGEs/sRAGE ratio. CRP was associated with the AGEs/sRAGE ratio while PEW showed no associations with AGEs–RAGE components or MDP. Conclusions. CKD is characterized by increased glycoxidative stress and reduced MDPs, reflecting altered mitochondrial stress signaling. AGEs–RAGE and MDPs are biologically linked, suggesting partially overlapping but distinct pathophysiological pathways. Full article
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