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Redox Homeostasis and Oxidative Stress in Human Metabolism and Disease：2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 3084

Special Issue Editors

Prof. Dr. Alina Woźniak

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Guest Editor
Department of Medical Biology and Biochemistry, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 24 Karłowicza St., 85-092 Bydgoszcz, Poland
Interests: reactive oxygen species; oxidative stress; antioxidants; lipid peroxidation; exercise biochemistry; cryostimulation; parasitology
Special Issues, Collections and Topics in MDPI journals
Dr. Jaroslaw Nuszkiewicz

E-Mail Website
Guest Editor
Department of Medical Biology and Biochemistry, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 24 Karłowicza St., 85-092 Bydgoszcz, Poland
Interests: reactive oxygen species; oxidative stress; antioxidants; oncology; metabolic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The finely tuned equilibrium of redox reactions forms the bedrock of many cellular functions underlying key metabolic processes and influencing the health of tissues and organs. This balance, critical for cell functionality, is frequently compromised in a myriad of diseases, including metabolic disorders, degenerative conditions and various other pathophysiological states. Perturbations in redox homeostasis often result from an imbalance between the production of reactive oxygen species (ROS) and antioxidant response mechanisms. At physiological levels, ROS serve as pivotal signaling molecules in a wide range of metabolic activities. However, excessive ROS accumulation can deleteriously perturb metabolic functions, instigating a diseased state and accelerating its progression. Furthermore, the intimate relationship between redox dynamics and human metabolism becomes even more complex when considering the influence of exogenous factors. These agents, in varied concentrations, can either maintain a redox equilibrium, thereby aiding metabolic function, or disrupt it, exacerbating oxidative stress. A deeper grasp of these multifaceted interactions is crucial not only for understanding disease etiology, but also devising innovative therapeutic interventions and preventive measures.

In this vein, this Special Issue invites submissions of original research articles that shed light on the intricate dance of redox signaling within metabolic contexts, both in health and disease. Articles highlighting the potential therapeutic strategies targeting redox imbalances in metabolic disorders are particularly encouraged. Additionally, comprehensive review articles that evaluate and dissect the current knowledge landscape pertaining to the theme are most welcome.

Prof. Dr. Alina Woźniak
Dr. Jaroslaw Nuszkiewicz
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • antioxidants
  • biomarkers
  • cellular functions
  • disease etiology
  • disease progression
  • metabolic disorders
  • metabolic signaling
  • oxidative stress
  • pathophysiological states
  • reactive oxygen species
  • redox homeostasis
  • redox signaling

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Published Papers (5 papers)

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Research

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10 pages, 1783 KiB  
Communication
Protection of Mitochondria, Cells and Organs from Ischemia–Reperfusion Damage Through Preventive Redox Bioregulation by Ozone
by Renate Viebahn-Haensler and Olga Sonia León Fernández
Int. J. Mol. Sci. 2025, 26(12), 5557; https://doi.org/10.3390/ijms26125557 - 10 Jun 2025
Viewed by 184
Abstract
Ischemia–reperfusion (I/R) damage remains a major problem in surgery, primarily based on high oxidative stress generated during the reperfusion process. Mitochondria are significantly affected, their metabolic and energetic processes are impaired, and the redox system is out of balance. Regulation and restoration of [...] Read more.
Ischemia–reperfusion (I/R) damage remains a major problem in surgery, primarily based on high oxidative stress generated during the reperfusion process. Mitochondria are significantly affected, their metabolic and energetic processes are impaired, and the redox system is out of balance. Regulation and restoration of the redox balance by oxidative preconditioning with ozone is being investigated worldwide in cell and animal models. Selected preclinical trials and their results, with a focus on cardiological and neuronal I/R damage, are presented and discussed. We regularly find an upregulation of antioxidants, demonstrated in SOD (superoxide dismutase) and GSH (glutathione, reduced form, and a decrease in oxidative stress as a result, shown here using the typical stress parameters, MDA (malondialdehyde) and TBARS (thiobarbituric acid reactive substances). Mitochondrial biogenesis, comparable to moderate physical activity, is induced by ozone oxidative preconditioning in an I/R model in rats and reviewed in this paper. Full article
(This article belongs to the Special Issue Redox Homeostasis and Oxidative Stress in Human Metabolism and Disease：2nd Edition)
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15 pages, 280 KiB  
Article
SII, SIRI, and MHR as Additional Readings for Personalized Evaluation of Chronic Heart Failure Severity
by Edis Baubonis, Jolanta Laukaitienė, Ingrida Grabauskytė and Aušra Mongirdienė
Int. J. Mol. Sci. 2025, 26(11), 5190; https://doi.org/10.3390/ijms26115190 - 28 May 2025
Viewed by 284
Abstract
(1) The aim of the study was to reveal what differences in patients’ lipidogram, oxidative stress, and echocardiographic readings are reflected by SII, SIRI, and MHR of the patients with chronic heart failure (CHF). (2) A total of 220 patients diagnosed with CHF [...] Read more.
(1) The aim of the study was to reveal what differences in patients’ lipidogram, oxidative stress, and echocardiographic readings are reflected by SII, SIRI, and MHR of the patients with chronic heart failure (CHF). (2) A total of 220 patients diagnosed with CHF were investigated. They were stratified into groups according to averages of SII (neutrophil * platelet/lymphocyte count), SII ≤ 684.757 (n = 115), and SII > 684.757 (n = 62); SIRI (neutrophil * monocyte/lymphocyte count), SIRI ≤ 2.098 (n = 110), SIRI > 2.098 (n = 67); and monocyte count/high-density lipoprotein cholesterol concentration (MHR), MHR ≤ 0.5854 (n = 54), and MHR > 0.5854 (n = 64) values. The analysis of transthoracic echocardiogram, complete blood count test, C reactive protein, lipidogram, oxHDL, nitrotirozine, ditirozine, TAC, protein carbonyl, catalase, and MDA were performed; (3) Between the groups, according to SII and SIRI, there were no statistically significant differences in lipidogram, oxidative stress, and echocardiography readings. In those with higher MHR, HDL concentration was lower (0.91 (0.44; 1.45) and 1.27 (0.72; 2.69), p < 0.001). In those with higher MHR, LVEDD was higher (58.12 (10.03) and 51.53 (10.34), p < 0.001), LVMM was higher (274.92 (92.24) and 233.07 (74.84), p = 0.010), MMI was higher (130.88 (34.28; 227.97) and 114.27 (70.34; 270.00), p = 0.022), and LVEF was lower (28.5 (10.0; 55.0) and 40.0 (20.0; 55.0), p < 0.001). MHR correlated with MMI (r = 0.287, p = 0.028) and LVMI (r = 0.287, p = 0.028). Nitrotyrosine concentration was higher in those with higher MHR (4.52 (1.12; 93.58) and 3.52 (1.74; 28.32), p = 0.022). MHR correlated with protein carbonyl (r = 0.321, p = 0.013), nitrotyrosine concentration (r = 0.356, p = 0.006). SIRI correlated with carbonyl protein concentration (r = 0.321, p = 0.013); (4) 1. In CHF patients, MHR could reflect the worsening of patients’ conditions related to oxidative stress. 2. The possibility to use SII and SIRI still needs to be confirmed. Full article
(This article belongs to the Special Issue Redox Homeostasis and Oxidative Stress in Human Metabolism and Disease：2nd Edition)

Review

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15 pages, 1124 KiB  
Review
Prolonged Intestinal Ethanol Absorption and Oxidative Stress: Revisiting the Gut–Liver Axis in Alcohol-Associated Disease
by Beom Sun Chung, Keungmo Yang, Chihyun Park and Tom Ryu
Int. J. Mol. Sci. 2025, 26(12), 5442; https://doi.org/10.3390/ijms26125442 - 6 Jun 2025
Viewed by 223
Abstract
Chronic alcohol consumption induces oxidative stress not only in the liver but also in the gastrointestinal tract, where prolonged intestinal ethanol absorption plays a pivotal and underrecognized role. This review reframes ethanol pharmacokinetics to emphasize sustained jejunal and ileal uptake, which maintains elevated [...] Read more.
Chronic alcohol consumption induces oxidative stress not only in the liver but also in the gastrointestinal tract, where prolonged intestinal ethanol absorption plays a pivotal and underrecognized role. This review reframes ethanol pharmacokinetics to emphasize sustained jejunal and ileal uptake, which maintains elevated blood alcohol levels and perpetuates redox imbalance across the gut–liver axis. We integrate recent findings on ethanol-induced barrier dysfunction, CYP2E1-mediated ROS production, microbial dysbiosis, and mitochondrial disruption, proposing that the intestine is an active site of injury and a driver of systemic inflammation. Key mechanistic insights reveal that gut-derived endotoxins, compromised epithelial integrity, and microbiome–mitochondria interactions converge to exacerbate hepatic and extrahepatic damage. We further explore emerging therapeutic strategies—ranging from NAD+ repletion and probiotics to fecal microbiota transplantation—that target this upstream pathology. Recognizing prolonged intestinal ethanol absorption as a clinically meaningful phase offers new directions for early intervention and redox-based treatment in alcohol-associated disease. Full article
(This article belongs to the Special Issue Redox Homeostasis and Oxidative Stress in Human Metabolism and Disease：2nd Edition)
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25 pages, 1144 KiB  
Review
Oxidative Stress and Endothelial Dysfunction: The Pathogenesis of Pediatric Hypertension
by Kyle Backston, Jordan Morgan, Samipa Patel, Riddhima Koka, Jieji Hu and Rupesh Raina
Int. J. Mol. Sci. 2025, 26(11), 5355; https://doi.org/10.3390/ijms26115355 - 3 Jun 2025
Viewed by 479
Abstract
Pediatric hypertension is increasingly recognized as a complex condition shaped by both systemic and cellular factors, with oxidative stress emerging as a key driver of vascular dysfunction. In both their primary and secondary forms, reactive oxygen species (ROS) disrupt redox homeostasis, impair endothelial [...] Read more.
Pediatric hypertension is increasingly recognized as a complex condition shaped by both systemic and cellular factors, with oxidative stress emerging as a key driver of vascular dysfunction. In both their primary and secondary forms, reactive oxygen species (ROS) disrupt redox homeostasis, impair endothelial signaling, and promote inflammation and tissue remodeling. Metabolic dysregulation, renal pathology, and early-life stressors contribute to the accumulation of ROS through pathways involving NADPH oxidases, mitochondrial dysfunction, xanthine oxidase activity, and altered arginine metabolism. These mechanisms converge on the vasculature, diminishing nitric oxide bioavailability and promoting hypertensive phenotypes. Beyond disease initiation, redox imbalance influences the response to treatment, surgical outcomes, and long-term cardiovascular risk. By further elucidating these mechanisms, the complex relationship between oxidative stress, vascular biology, and blood pressure regulation in children may be more clearly defined and more effectively targeted in clinical management. Full article
(This article belongs to the Special Issue Redox Homeostasis and Oxidative Stress in Human Metabolism and Disease：2nd Edition)
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21 pages, 542 KiB  
Review
Antioxidant Therapies as Emerging Adjuncts in Rheumatoid Arthritis: Targeting Oxidative Stress to Enhance Treatment Outcomes
by Rafał Bilski and Jarosław Nuszkiewicz
Int. J. Mol. Sci. 2025, 26(7), 2873; https://doi.org/10.3390/ijms26072873 - 21 Mar 2025
Cited by 1 | Viewed by 1058
Abstract
Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent inflammation and progressive joint destruction. Recent data underscore oxidative stress as a primary factor in the pathophysiology of rheumatoid arthritis, intensifying inflammatory processes and tissue damage via the overproduction of reactive oxygen [...] Read more.
Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent inflammation and progressive joint destruction. Recent data underscore oxidative stress as a primary factor in the pathophysiology of rheumatoid arthritis, intensifying inflammatory processes and tissue damage via the overproduction of reactive oxygen species (ROS) and compromised antioxidant defenses. Current therapies, including disease-modifying antirheumatic drugs (DMARDs), primarily target immune dysregulation but fail to address oxidative stress, necessitating novel adjunctive treatment strategies. This review explores the potential of antioxidant-based therapies as complementary approaches to RA management. Natural compounds such as curcumin, resveratrol, sulforaphane, and propolis exhibit strong anti-inflammatory and antioxidative properties by modulating redox-sensitive pathways, including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear factor erythroid 2-related factor 2(Nrf2)/heme oxygenase (HO-1). N-acetylcysteine (NAC) replenishes intracellular glutathione, enhancing cellular resilience against oxidative stress. Additionally, molecular hydrogen (H2) selectively neutralizes harmful ROS, reducing oxidative damage and inflammation. The role of vitamin supplementation (D, B12, C, and K) in regulating immune responses and protecting joint structures is also discussed. This review aims to evaluate the efficacy and potential clinical applications of antioxidant therapies in RA, emphasizing their role in mitigating oxidative damage and improving treatment outcomes. While preliminary findings are promising, further clinical trials are needed to establish standardized dosing, long-term safety, and their integration into current RA treatment protocols. Full article
(This article belongs to the Special Issue Redox Homeostasis and Oxidative Stress in Human Metabolism and Disease：2nd Edition)
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