Oxidative Stress and Mitochondrial Dysfunction in Metabolic and Inflammatory Diseases

Topic Information

Dear Colleagues,

Background Intracellular oxidative stress is induced by the overexpression of reactive oxygen species (ROS) and/or decreased antioxidants defense activity, causing deleterious chemical changes in biomolecules, such as lipids, DNA/RNA, and proteins. ROS are the highly reactive, oxygen-containing, radical or molecular species that include superoxide anion/radical (O2•‒), hydrogen peroxide (H2O2), and hydroxyl radical (HO•). Chemically, ROS are generated from molecular oxygen (O2) during the successive four steps of one electron reduction in mitochondrial respiratory chain. Free radicals (O2•‒/HO•) can further react with organic substrates to form intermediate species and yield the secondary ROS, such as peroxyl radical (RO2•) and hydroperoxide (ROOH). H2O2, which is a relatively less toxic but more stable molecular species, becomes highly toxic after further interaction with Fe++ (Fenton reaction) or in presence of O2•‒ (Haber-Weiss reaction). Scope and information for Authors Obesity triggers the risk of metabolic syndromes including hypertension, type 2 diabetes and related morbidities, such as hypertension, atherosclerosis, NAFLD/NASH, stroke, cardiovascular disease, aging, neurodegenerative diseases, certain types of cancers, and other chronic inflammatory conditions. Over the past years, significant progress has been made toward developing therapeutic strategies, pharmacological interventions, and mitochondria-targeted approaches that reduce oxidative stress and mitochondrial damage and dysfunction and improve mitochondrial quality in disease setting. The purpose of this Special Issue is to highlight the recent advances and progress on the mechanisms of ROS-mediated oxidative stress and mitochondrial dysfunction, as well as novel therapeutic strategies used in metabolic and inflammatory diseases. We, therefore, we welcome original research, review, mini review, and perspective articles on above-mentioned pathophysiological changes in setting of: obesity; diabetes; hypertension; NAFLD/NASH; stroke; atherosclerosis; cardiovascular disease; aging and age-related neurodegenerative diseases; and other chronic inflammatory conditions. Goal About 90% of the endogenous ROS are generated during oxidative phosphorylation in the mitochondria which are the powerhouses to provide energy to cell in the form of ATP molecules, in order to fuel biochemical reactions and support biological functions. In addition to the ATP synthesis and ROS production/scavenging, mitochondria also regulate intracellular Ca2+, apoptotic cell death, and activation of the caspase family of proteases. ROS accumulation, whether from overproduction or as a sequel to defective antioxidant enzymes may lead to the irreversible damage to mitochondria, which may induce or exacerbate pathologies across a wider spectrum of metabolic and inflammatory diseases. The goal is to enhance our understanding how the ROS play out in physiology and pathophysiology, and how the ROS imbalance may influence the cellular or tissue homeostasis and critical cellular processes, such as aerobic/anaerobic respiration, β-oxidation, fatty acid synthesis, protein translation and post-translational modifications, and other modifications driving the genetic/epigenetic landscape reprogramming in metabolic and inflammatory diseases.

Dr. Sardar Sindhu
Dr. Fahd Al-Mulla
Dr. Rasheed Ahmad
Dr. José Antonio Morales-González
Topic Editors

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Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Cells cells	7.666	6.7	2012	16.4 Days	2400 CHF	Submit
Endocrines endocrines	-	-	2020	27.5 Days	1000 CHF	Submit
Journal of Molecular Pathology jmp	-	-	2020	13.5 Days	1000 CHF	Submit
Metabolites metabolites	5.581	4.7	2011	12.9 Days	2200 CHF	Submit
Stresses stresses	-	-	2021	19.6 Days	1000 CHF	Submit
Current Issues in Molecular Biology cimb	2.976	2.7	1999	17.2 Days	2000 CHF	Submit

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All Cells Endocrines JMP Metabolites Stresses CIMB

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Open AccessReview

Natural Mitochondria Targeting Substances and Their Effect on Cellular Antioxidant System as a Potential Benefit in Mitochondrial Medicine for Prevention and Remediation of Mitochondrial Dysfunctions

by

Daniel Schniertshauer

,

Susanne Wespel

and

Jörg Bergemann

Curr. Issues Mol. Biol. 2023, 45(5), 3911-3932; https://doi.org/10.3390/cimb45050250 - 02 May 2023

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Abstract

Based on the knowledge that many diseases are caused by defects in the metabolism of the cells and, in particular, in defects of the mitochondria, mitochondrial medicine starts precisely at this point. This new form of therapy is used in numerous fields of [...] Read more.

Based on the knowledge that many diseases are caused by defects in the metabolism of the cells and, in particular, in defects of the mitochondria, mitochondrial medicine starts precisely at this point. This new form of therapy is used in numerous fields of human medicine and has become a central focus within the field of medicine in recent years. With this form of therapy, the disturbed cellular energy metabolism and an out-of-balance antioxidant system of the patient are to be influenced to a greater extent. The most important tool here is mitotropic substances, with the help of which attempts are made to compensate for existing dysfunction. In this article, both mitotropic substances and accompanying studies showing their efficacy are summarized. It appears that the action of many mitotropic substances is based on two important properties. First, on the property of acting antioxidantly, both directly as antioxidants and via activation of downstream enzymes and signaling pathways of the antioxidant system, and second, via enhanced transport of electrons and protons in the mitochondrial respiratory chain. Full article

(This article belongs to the Topic Oxidative Stress and Mitochondrial Dysfunction in Metabolic and Inflammatory Diseases)

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Open AccessArticle

Elicitation of Inhibitory Effects for AGE-Induced Oxidative Stress in Rotator Cuff-Derived Cells by Apocynin

by

Takahiro Furukawa

,

Takashi Kurosawa

,

Yutaka Mifune

,

Atsuyuki Inui

,

Hanako Nishimoto

,

Yasuhiro Ueda

,

Takeshi Kataoka

,

Kohei Yamaura

,

Shintaro Mukohara

,

Tomoya Yoshikawa

,

Issei Shinohara

,

Tatsuo Kato

,

Shuya Tanaka

,

Masaya Kusunose

,

Yuichi Hoshino

,

Takehiko Matsushita

and

Ryosuke Kuroda

Curr. Issues Mol. Biol. 2023, 45(4), 3434-3445; https://doi.org/10.3390/cimb45040225 - 14 Apr 2023

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Abstract

Advanced glycation end-products (AGEs) play a critical supportive role during musculoskeletal disorders via glycosylation and oxidative stress. Though apocynin, identified as a potent and selective inhibitor of NADPH oxidase, has been reported to be involved in pathogen-induced reactive oxygen species (ROS), its role [...] Read more.

Advanced glycation end-products (AGEs) play a critical supportive role during musculoskeletal disorders via glycosylation and oxidative stress. Though apocynin, identified as a potent and selective inhibitor of NADPH oxidase, has been reported to be involved in pathogen-induced reactive oxygen species (ROS), its role in age-related rotator cuff degeneration has not been well clarified. Therefore, this study aims to evaluate the in vitro effects of apocynin on human rotator cuff-derived cells. Twelve patients with rotator cuff tears (RCTs) participated in the study. Supraspinatus tendons from patients with RCTs were collected and cultured. After the preparation of RC-derived cells, they were divided into four groups (control group, control + apocynin group, AGEs group, AGEs + apocynin group), and gene marker expression, cell viability, and intracellular ROS production were evaluated. The gene expression of NOX, IL-6, and the receptor for AGEs (RAGE) was significantly decreased by apocynin. We also examined the effect of apocynin in vitro. The results showed that ROS induction and increasing apoptotic cells after treatment of AGEs were significantly decreased, and cell viability increased considerably. These results suggest that apocynin can effectively reduce AGE-induced oxidative stress by inhibiting NOX activation. Thus, apocynin is a potential prodrug in preventing degenerative changes of the rotor cuff. Full article

(This article belongs to the Topic Oxidative Stress and Mitochondrial Dysfunction in Metabolic and Inflammatory Diseases)

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Open AccessOpinion

Rheumatoid Arthritis and Reactive Oxygen Species: A Review

by

Naoki Kondo

,

Tomotake Kanai

and

Masayasu Okada

Curr. Issues Mol. Biol. 2023, 45(4), 3000-3015; https://doi.org/10.3390/cimb45040197 - 03 Apr 2023

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Abstract

Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disease that causes progressive joint damage and can lead to lifelong disability. Numerous studies support the hypothesis that reactive oxygen species (ROS) are associated with RA pathogenesis. Recent advances have clarified the anti-inflammatory effect of [...] Read more.

Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disease that causes progressive joint damage and can lead to lifelong disability. Numerous studies support the hypothesis that reactive oxygen species (ROS) are associated with RA pathogenesis. Recent advances have clarified the anti-inflammatory effect of antioxidants and their roles in RA alleviation. In addition, several important signaling pathway components, such as nuclear factor kappa B, activator-protein-1, nuclear factor (erythroid-derived 2)-like 2/kelch-like associated protein, signal transducer and activator of transcription 3, and mitogen-activated protein kinases, including c-Jun N-terminal kinase, have been identified to be associated with RA. In this paper, we outline the ROS generation process and relevant oxidative markers, thereby providing evidence of the association between oxidative stress and RA pathogenesis. Furthermore, we describe various therapeutic targets in several prominent signaling pathways for improving RA disease activity and its hyper oxidative state. Finally, we reviewed natural foods, phytochemicals, chemical compounds with antioxidant properties and the association of microbiota with RA pathogenesis. Full article

(This article belongs to the Topic Oxidative Stress and Mitochondrial Dysfunction in Metabolic and Inflammatory Diseases)

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Open AccessArticle

The Impact of Krebs Cycle Intermediates on the Endocrine System and Immune System: A Comparison

by

Borros M. Arneth

Endocrines 2023, 4(1), 179-193; https://doi.org/10.3390/endocrines4010016 - 08 Mar 2023

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Abstract

Introduction: The Krebs cycle is an important set of reactions that synthesize different molecules and substances that affect various organs. The objective of this paper was to compare the effects of Krebs cycle intermediates on the endocrine system and the immune system. Methods [...] Read more.

Introduction: The Krebs cycle is an important set of reactions that synthesize different molecules and substances that affect various organs. The objective of this paper was to compare the effects of Krebs cycle intermediates on the endocrine system and the immune system. Methods and Materials: The articles used in this paper were obtained from a systematic search of PsycINFO, PubMed, Web of Science, CINAHL, and primary databases. The search terms were “Krebs cycle,” “intermediates,” “endocrine system,” “tricarboxylic acid,” “citric acid cycle,” and “immune system,” and Boolean operators (AND/OR) were used to combine terms. Results: A review of the selected studies showed that Krebs cycle intermediates influence how the endocrine system regulates and controls body processes, including energy uptake. Moreover, these intermediates have both direct and indirect effects on immune function, memory, and activation. Discussion: An understanding of the effects of Krebs cycle intermediates on endocrine and immune processes will provide valuable insights for the development of new therapies. Additionally, this knowledge is a basis for exploring the pathogenesis of the complications related to endocrine system function and for evaluating the immune system response to pathogens. Conclusions: The evidence gathered in this review shows that Krebs cycle intermediates have significant effects on immune and endocrine processes. However, further human and in vivo studies are required to generate additional evidence for the underlying pathways and to identify the potential strategies for targeting these mechanisms to manage specific disorders. Full article

(This article belongs to the Topic Oxidative Stress and Mitochondrial Dysfunction in Metabolic and Inflammatory Diseases)

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