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Oxidative Stress and Metabolic Diseases
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Oxidative Stress and Metabolic Diseases

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: closed (31 July 2023) | Viewed by 14642

Special Issue Editor

Dr. Daniele Vergara

E-Mail Website
Guest Editor
Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Italy
Interests: cellular physiology; proteomics; cell plasticity; epithelial to mesenchymal transition; signal transduction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Metabolic diseases occur when normal metabolic processes in the body are disrupted. These diseases can include a variety of ailments, such as insulin resistance, dyslipidemia, type 2 diabetes, cardiovascular disease, and cancer. Alterations in different classes of signaling molecules play an important role in the onset of metabolic diseases. In this scenario, reactive molecules, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), are crucial regulators of metabolic homeostasis. Many studies support the hypothesis that oxidative stress plays a significant role in the development of metabolic disorders, particularly insulin resistance, and the treatment of oxidative stress can improve insulin sensitivity, hyperlipidemia, or fatty liver, preventing associated metabolic complications.

Although physiological concentrations of ROS and RNS can act as second messengers in adaptive stress responses, their overproduction could be detrimental to many cellular constituents, such as proteins, lipids, and nucleic acids. Incorrect nutritional habits, such as a diet rich in fats and/or carbohydrates, can promote oxidative stress, with a concomitant increase in lipid and protein peroxidation and a reduction in antioxidant defenses. Additionally, the increased oxidative environment contributes to a chronic inflammatory condition which, in turn, can cause the inflammatory condition to progress and be sustained by creating a vicious cycle.

Understanding the role played by ROS and RNS in cell physiology has led to the development of new biomarkers and molecular targets that could be useful in the development of innovative approaches in the prevention, diagnosis, and treatment of inflammatory and metabolic diseases. Furthermore, ongoing intensive research in this area is providing new information that is vital to further advance our understanding of this complex field.

Papers addressing these topics are invited for this Special Issue, especially those combining the relation of oxidative stress and nutrition in the prevention or the treatment of metabolic disorders.

Dr. Daniele Vergara
Guest Editor

Manuscript Submission Information

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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

  • cancer
  • cardiovascular diseases
  • inflammation
  • diabetes
  • metabolic disorders
  • oxidative stress
  • reactive oxygen species
  • physiology

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Published Papers (2 papers)

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12 pages, 1618 KiB  
Article
Metabolic Syndrome as a Factor of Impairment of Antioxidant Defense System in Youth with T1DM
by Monika Grabia, Katarzyna Socha, Artur Bossowski and Renata Markiewicz-Żukowska
Int. J. Mol. Sci. 2023, 24(11), 9428; https://doi.org/10.3390/ijms24119428 - 29 May 2023
Cited by 1 | Viewed by 1765
Abstract
Research indicates that adolescents with type 1 diabetes mellitus (T1DM) may develop both metabolic syndrome (MetS) and oxidative stress. The purpose of this study was to test the hypothesis that MetS could potentially affect antioxidant defense parameters. The study recruited adolescents aged 10–17 [...] Read more.
Research indicates that adolescents with type 1 diabetes mellitus (T1DM) may develop both metabolic syndrome (MetS) and oxidative stress. The purpose of this study was to test the hypothesis that MetS could potentially affect antioxidant defense parameters. The study recruited adolescents aged 10–17 who had been diagnosed with T1DM, and divided them into two groups: “MetS+” (n = 22), who had been diagnosed with MetS, and “MetS−” (n = 81), who did not have metabolic syndrome. A control group consisting of 60 healthy peers without T1DM was included for comparison. The study examined cardiovascular parameters, such as complete lipid profile and estimated glucose disposal rate (eGDR), as well as markers of antioxidant defense. The results revealed a statistically significant difference between the MetS+ and the MetS− group in terms of total antioxidant status (TAS) (1.186 mmol/L vs. 1.330 mmol/L), and oxidative stress index (OSI) levels (0.666 vs. 0.533). Furthermore, multivariate correspondence analysis identified individuals with HbA1c < 8%; eGDR > 8 mg/kg/min, using either flash or continuous glucose monitoring systems, as MetS− patients. The study also found that eGDR (AUC 0.85, p < 0.001), OSI and HbA1c (AUC 0.71, p < 0.001) markers may be useful for diagnosing the onset of MetS in adolescents with T1DM. Full article
(This article belongs to the Special Issue Oxidative Stress and Metabolic Diseases)
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Review

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17 pages, 1166 KiB  
Review
Lipid Peroxidation and Iron Metabolism: Two Corner Stones in the Homeostasis Control of Ferroptosis
by Luc Rochette, Geoffrey Dogon, Eve Rigal, Marianne Zeller, Yves Cottin and Catherine Vergely
Int. J. Mol. Sci. 2023, 24(1), 449; https://doi.org/10.3390/ijms24010449 - 27 Dec 2022
Cited by 220 | Viewed by 12075
Abstract
Regulated cell death (RCD) has a significant impact on development, tissue homeostasis, and the occurrence of various diseases. Among different forms of RCD, ferroptosis is considered as a type of reactive oxygen species (ROS)-dependent regulated necrosis. ROS can react with polyunsaturated fatty acids [...] Read more.
Regulated cell death (RCD) has a significant impact on development, tissue homeostasis, and the occurrence of various diseases. Among different forms of RCD, ferroptosis is considered as a type of reactive oxygen species (ROS)-dependent regulated necrosis. ROS can react with polyunsaturated fatty acids (PUFAs) of the lipid (L) membrane via the formation of a lipid radical L• and induce lipid peroxidation to form L-ROS. Ferroptosis is triggered by an imbalance between lipid hydroperoxide (LOOH) detoxification and iron-dependent L-ROS accumulation. Intracellular iron accumulation and lipid peroxidation are two central biochemical events leading to ferroptosis. Organelles, including mitochondria and lysosomes are involved in the regulation of iron metabolism and redox imbalance in ferroptosis. In this review, we will provide an overview of lipid peroxidation, as well as key components involved in the ferroptotic cascade. The main mechanism that reduces ROS is the redox ability of glutathione (GSH). GSH, a tripeptide that includes glutamic acid, cysteine, and glycine, acts as an antioxidant and is the substrate of glutathione peroxidase 4 (GPX4), which is then converted into oxidized glutathione (GSSG). Increasing the expression of GSH can inhibit ferroptosis. We highlight the role of the xc- GSH-GPX4 pathway as the main pathway to regulate ferroptosis. The system xc-, composed of subunit solute carrier family members (SLC7A11 and SLC3A2), mediates the exchange of cystine and glutamate across the plasma membrane to synthesize GSH. Accumulating evidence indicates that ferroptosis requires the autophagy machinery for its execution. Ferritinophagy is used to describe the removal of the major iron storage protein ferritin by the autophagy machinery. Nuclear receptor coactivator 4 (NCOA4) is a cytosolic autophagy receptor used to bind ferritin for subsequent degradation by ferritinophagy. During ferritinophagy, stored iron released becomes available for biosynthetic pathways. The dysfunctional ferroptotic response is implicated in a variety of pathological conditions. Ferroptosis inducers or inhibitors targeting redox- or iron metabolism-related proteins and signal transduction have been developed. The simultaneous detection of intracellular and extracellular markers may help diagnose and treat diseases related to ferroptotic damage. Full article
(This article belongs to the Special Issue Oxidative Stress and Metabolic Diseases)
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