Metabolic Enzymes of Thrombo-Inflammatory and Oxidative Stress Mediators in Health and Disease

A special issue of Catalysts (ISSN 2073-4344). This special issue belongs to the section "Biocatalysis".

Deadline for manuscript submissions: 15 May 2025 | Viewed by 937

Special Issue Editors


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Guest Editor
Hephaestus Laboratory, School of Chemistry, Faculty of Sciences, Democritus University of Thrace, Kavala University Campus, 65404 Kavala, Greece
Interests: anti-inflammatory; antithrombotic; antiplatelet; bioactives; bioanalytical chemistry
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Special Issue Information

Dear Colleagues,

Inflammation, thrombosis and oxidative stress are implicated in several physiological processes; but, if dysregulated and thus unresolved, then according to the WHO and the current literature, these processes can lead to unfavorable pathological manifestations and associated disorders. Specific mediators, the levels of which are tightly regulated by specific enzyme machinery, are involved in the main signaling cascades of these processes. The main regulatory enzymes for the synthesis and/or catabolism of important thrombo-inflammatory mediators are affected by the disease state and can thus can either increase and prolong the levels of the mediators they synthesize and/or they can decrease or cause the withdrawal of these/other mediators involved. As with other biological processes, the dynamic aspects of the biochemistry of enzymes that interfere in the inflammation process are complicated and thus they require further evaluation and, in some cases, thorough re-assessment.

The aim of the specific Special Issue is to shed light on the current status, advances, interactions, conflicts and future perspectives of the roles of inducible enzymes in health and disease that are involved in inflammation, thrombosis and oxidative stress, such as several pro-inflammatory enzymes like cyclooxygenase (COX) and lipoxygenase (LOX) that induce synthesis from arachidonic acid (AA)-derived bioactive lipids, prostanoids and leukotrienes, respectively, collectively called eicosanoids. These are targets for several non-steroidal anti-inflammatory drugs/pharmaceuticals, as well as nitric oxide synthase (iNOS), aldo-keto reductases (AKRs), glutathione transferases (GSTs), metalloproteinases (MMPs) and several other pro-/anti-inflammatory enzymes like the synthetic and catabolic enzymes of several other important thrombo-inflammatory mediators like platelet activating factor (PAF)—the dysregulation of which is involved in several pathological situations. There are also pro-oxidant and/or antioxidant enzymes involved in oxidative stress-related manifestations like superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), nitric oxide synthase (eNOS, iNOS, and nNOS), peroxiredoxins, thioredoxins (Trx), and more.

Research articles, comprehensive and/or critical, and/or systematic reviews and meta-analysis studies on the above are welcomed to be submitted to this interesting Special Issue.

Dr. Alexandros Tsoupras
Dr. Anna Ofrydopoulou
Guest Editors

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Keywords

  • inflammation
  • thrombosis
  • oxidative stress
  • metabolic enzymes
  • cyclooxygenases
  • regulatory enzymes
  • anti-inflammatory
  • antithrombotic
  • antioxidant

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Published Papers (1 paper)

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Review

20 pages, 3241 KiB  
Review
Superoxide Dismutase Glycation: A Contributor to Disease and Target for Prevention
by Masood Alam Khan and Hina Younus
Catalysts 2025, 15(3), 247; https://doi.org/10.3390/catal15030247 - 5 Mar 2025
Viewed by 712
Abstract
Superoxide dismutase (SOD), a key antioxidant enzyme, plays a crucial role in neutralizing reactive oxygen species (ROS) and maintaining redox balance. However, SOD is highly susceptible to glycation, a non-enzymatic modification induced by reducing sugars and reactive carbonyl species such as methylglyoxal. This [...] Read more.
Superoxide dismutase (SOD), a key antioxidant enzyme, plays a crucial role in neutralizing reactive oxygen species (ROS) and maintaining redox balance. However, SOD is highly susceptible to glycation, a non-enzymatic modification induced by reducing sugars and reactive carbonyl species such as methylglyoxal. This review aims to provide a comprehensive analysis of SOD glycation, examining its biochemical mechanisms, its impact on enzymatic function, and its role in the progression of oxidative stress-related diseases. Additionally, it explores potential therapeutic strategies to prevent SOD glycation and restore its activity, highlighting translational applications for disease management. The review examines research on SOD glycation and its pathological consequences in diabetes complications, neurodegenerative disorders, and cardiovascular diseases. Key therapeutic interventions, including advanced glycation end-product (AGE) inhibitors (aminoguanidine, pyridoxamine), antioxidants (N-acetylcysteine, alpha-lipoic acid), SOD mimetics (MnTBAP, Tempol), enzyme stabilizers (thymoquinone, alliin), and receptor for advanced glycation end-products (RAGE) blockade, are analyzed for their efficacy in mitigating oxidative stress. SOD glycation reduces enzymatic activity, leading to elevated ROS levels and inflammation. Glycated SOD interacts with RAGE, increasing oxidative stress biomarkers. AGE inhibitors reduce carbonyl stress, whereas antioxidants lower ROS levels. SOD mimetics restore up to 85% of enzymatic activity, and enzyme stabilizers protect SOD from structural degradation. Additionally, monoclonal antibodies targeting RAGE have been shown to reduce inflammatory cytokines and improve mitochondrial function. SOD glycation is a major contributor to oxidative stress-related diseases. Preventing glycation and restoring SOD function through a multifaceted therapeutic approach is crucial for mitigating disease progression. By elucidating the role of SOD in disease pathogenesis, this review contributes to the advancement of targeted therapies for oxidative stress-related conditions, including diabetes, neurodegeneration, and cardiovascular diseases. Full article
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