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Antioxidants
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Oxidative Stress, Inflammation and Mitochondrial Dysfunction: Mutual Interactions in Obesity-Related...
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Oxidative Stress, Inflammation and Mitochondrial Dysfunction: Mutual Interactions in Obesity-Related Pathologies

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 15973

Special Issue Editors

Dr. Danina M. Muntean

E-Mail Website
Guest Editor
Department of Functional Sciences - Pathophysiology, “Victor Babeș” University of Medicine and Pharmacy, E. Murgu Sq. No. 2, 300041 Timișoara, Romania Center for Translational Research and Systems Medicine, “Victor Babeș” University of Medicine and Pharmacy, T. Vladimirescu No. 14, 300173 Timișoara, Romania
Interests: mitochondrial dysfunction; endothelial dysfunction; oxidative stress; monoamine oxidase; obesity; cardio-metabolic diseases
Dr. Seung-Hyun Ro

E-Mail Website
Guest Editor
Department of Biochemistry, University of Nebraska-Lincoln, 1901 Vine St. N217 Beadle Center, Lincoln, NE 68588-0664, USA Redox Biology Center, University of Nebraska-Lincoln, 1900 Vine St. N200 Beadle Center, Lincoln, NE 68588-0662, USA
Interests: adipocyte biology; autophagy; mitophagy; mitochondria metabolism; oxidative stress; sestrins/mTOR signaling

Special Issue Information

Dear Colleagues,

Obesity, also known as “adiposity-based chronic disease”, is a threatening ongoing pandemic that is unequivocally recognized as a state of chronic local and systemic oxidative stress.

The increased adipose tissue in obesity is a highly active yet dysfunctional metabolic organ that and acts as main stage for two other intricate mechanisms that underlie obesity pathogenesis, namely, low-grade inflammation and mitochondrial dysfunction.

Oxidative stress, inflammation and mitochondrial dysfunction are closely interconnected pathomechanisms that play critical roles in the etiology and progression of obesity and its related chronic pathologies.

Besides the hypertrophy and hyperplasia of white adipose tissues, obesity elicits the malfunction of thermogenesis and energy metabolism of brown adipose tissues in both animal models and humans. In adipose tissues, low physiological levels of reactive oxygen species (ROS) maintain cellular homeostasis by modulating the fat metabolism, mitochondrial function and secretion/release of inflammatory cytokines. At variance, high pathological levels of ROS and the associated oxidative stress damage molecules (proteins, lipids, nucleic acids) and intracellular organelles, including mitochondria. Therefore, targeting oxidative stress in adipose tissue and major metabolic tissues (e.g., liver, muscle, heart and brain) with antioxidants and/or redox-active compounds is the subject of a great deal of investigation with the aim of developing therapeutic approaches capable not only of decreasing ROS generation/increasing antioxidant defense but also eliciting an anti-inflammatory response and alleviating mitochondrial dysfunction. Additionally, specific anti-inflammatory agents or mitocan molecules can modulate intracellular and mitochondrial ROS as part of several metabolic pathways, as well as autophagy and apoptosis.

We invite you to submit your latest research findings and intuitive review articles to this Special Issue, which will bring together current research addressing the complex crosstalk between oxidative metabolism, inflammation and mitochondrial dysfunction and their significance in the pathophysiology of obesity and its complications. Research can include in vitro cell culture, as well as animal and human studies tackling any of the following topics: oxidative stress, antioxidants, redox metabolism, inflammation, mitochondrial stress, and adipose tissue dysfunction in the setting of obesity and its related pathologies.

We look forward to your contribution.

Dr. Danina M. Muntean
Dr. Seung-Hyun Ro
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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • oxidative stress
  • antioxidants
  • redox metabolism
  • inflammation
  • mitochondrial stress
  • adipose tissue dysfunction
  • obesity-related pathologies

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Published Papers (4 papers)

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Research

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14 pages, 3004 KiB  
Article
Metformin Impacts Human Syncytiotrophoblast Mitochondrial Function from Pregnancies Complicated by Obesity and Gestational Diabetes Mellitus in a Sexually Dimorphic Manner
by Jessica F. Hebert and Leslie Myatt
Antioxidants 2023, 12(3), 719; https://doi.org/10.3390/antiox12030719 - 14 Mar 2023
Cited by 6 | Viewed by 3471
Abstract
Maternal obesity and gestational diabetes mellitus (GDM) are associated with placental dysfunction, small for gestational age (SGA) offspring, and programming of adult-onset disease. We examine how metformin, commonly used to treat type A2 GDM, affects placental metabolism as well as mitochondrial content and [...] Read more.
Maternal obesity and gestational diabetes mellitus (GDM) are associated with placental dysfunction, small for gestational age (SGA) offspring, and programming of adult-onset disease. We examine how metformin, commonly used to treat type A2 GDM, affects placental metabolism as well as mitochondrial content and function. Syncytiotrophoblasts (STBs) were prepared from placentas of male and female fetuses collected at term cesarean section from lean (pre-pregnancy BMI < 25), obese (BMI > 30), and obese A2GDM women. Metformin treatment (0.001–10 mM) of STB caused no change in non-mitochondrial respiration but significant concentration-dependent (1 and 10 mM) decreases in basal, maximal, and ATP-linked respiration and spare capacity. Respiration linked to proton leak was significantly increased in STB of male A2GDM placentas at low metformin concentrations. Metformin concentrations ≥1 mM increased glycolysis in STB from placentas from lean women, but only improved glycolytic capacity in female STB. Whereas metformin had little effect on superoxide generation from male STB of any group, it gave a concentration-dependent decrease in superoxide generation from female STB of lean and obese women. Fewer mitochondria were observed in STB from obese women and male STB from lean women with increasing metformin concentration. Metformin affects STB mitochondrial function in a sexually dimorphic manner but at concentrations above those reported in maternal circulation (approximately 0.01 mM) in women treated with metformin for GDM. Full article
(This article belongs to the Special Issue Oxidative Stress, Inflammation and Mitochondrial Dysfunction: Mutual Interactions in Obesity-Related Pathologies)
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17 pages, 3698 KiB  
Article
Metallothionein 3 Inhibits 3T3-L1 Adipocyte Differentiation via Reduction of Reactive Oxygen Species
by Yuankuan Li, Sung Ho Lee, Meiyu Piao, Hyung Sik Kim and Kwang Youl Lee
Antioxidants 2023, 12(3), 640; https://doi.org/10.3390/antiox12030640 - 4 Mar 2023
Cited by 4 | Viewed by 3295
Abstract
Metallothionein 3 (MT3), also known as a neuronal growth-inhibitory factor, is a member of the metallothionein family and is involved in a variety of biological functions, including protection against metal toxicity and reactive oxygen species (ROS). However, less is known about the role [...] Read more.
Metallothionein 3 (MT3), also known as a neuronal growth-inhibitory factor, is a member of the metallothionein family and is involved in a variety of biological functions, including protection against metal toxicity and reactive oxygen species (ROS). However, less is known about the role of MT3 in the differentiation of 3T3-L1 cells into adipocytes. In this study, we observed that MT3 levels were downregulated during 3T3-L1 adipocyte differentiation. Mt3 overexpression inhibited adipocyte differentiation and reduced the levels of the adipogenic transcription factors C/EBPα and PPARγ. Further analyses showed that MT3 also suppressed the transcriptional activity of PPARγ, and this effect was not mediated by a direct interaction between MT3 with PPARγ. In addition, Mt3 overexpression resulted in a decrease in ROS levels during early adipocyte differentiation, while treatment with antimycin A, which induces ROS generation, restored the ROS levels. Mt3 knockdown, on the other hand, elevated ROS levels, which were suppressed upon treatment with the antioxidant N-acetylcysteine. Our findings indicate a previously unknown role of MT3 in the differentiation of 3T3-L1 cells into adipocytes and provide a potential novel target that might facilitate obesity treatment. Full article
(This article belongs to the Special Issue Oxidative Stress, Inflammation and Mitochondrial Dysfunction: Mutual Interactions in Obesity-Related Pathologies)
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18 pages, 4784 KiB  
Article
Bavachin and Corylifol A Improve Muscle Atrophy by Enhancing Mitochondria Quality Control in Type 2 Diabetic Mice
by Myeong-Hoon Yeon, Eunhui Seo, Jong-Han Lee and Hee-Sook Jun
Antioxidants 2023, 12(1), 137; https://doi.org/10.3390/antiox12010137 - 6 Jan 2023
Cited by 14 | Viewed by 3430
Abstract
Type 2 diabetes reduces muscle mass and function. Chronic inflammation and mitochondrial dysfunction play critical roles in muscle atrophy pathogenesis. Here, we investigated the effects of bavachin and corylifol A from Psoralea corylifolia L. seeds on muscle atrophy in dexamethasone-treated mice and in [...] Read more.
Type 2 diabetes reduces muscle mass and function. Chronic inflammation and mitochondrial dysfunction play critical roles in muscle atrophy pathogenesis. Here, we investigated the effects of bavachin and corylifol A from Psoralea corylifolia L. seeds on muscle atrophy in dexamethasone-treated mice and in db/db mice. Bavachin and corylifol A enhanced muscle strength and muscle mass in dexamethasone-treated mice. In diabetic mice, they enhanced muscle strength and cross-sectional areas. Bavachin and corylifol A suppressed inflammatory cytokine (interleukin-6 and tumor necrosis factor-α) expression levels by downregulating nuclear factor-κB phosphorylation. They decreased the muscle atrophic factor (myostatin, atrogin-1, and muscle RING finger-1) expression levels. They activated the AKT synthetic signaling pathway and induced a switch from fast-type glycolytic fibers (type 2B) to slow-type oxidative fibers (types I and 2A). They increased mitochondrial biogenesis and dynamic factor (optic atrophy-1, mitofusin-1/2, fission, mitochondrial 1, and dynamin 1-like) expression levels via the AMP-activated protein kinase–peroxisome proliferator-activated receptor gamma coactivator 1-alpha signaling pathway. They also improved mitochondrial quality by upregulating the mitophagy factor (p62, parkin, PTEN-induced kinase-1, and BCL2-interacting protein-3) expression levels. Therefore, bavachin and corylifol A exert potential therapeutic effects on muscle atrophy by suppressing inflammation and improving mitochondrial function. Full article
(This article belongs to the Special Issue Oxidative Stress, Inflammation and Mitochondrial Dysfunction: Mutual Interactions in Obesity-Related Pathologies)
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Review

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20 pages, 1301 KiB  
Review
Arsenic Toxicity on Metabolism and Autophagy in Adipose and Muscle Tissues
by Seung-Hyun Ro, Jiyoung Bae, Yura Jang, Jacob F. Myers, Soonkyu Chung, Jiujiu Yu, Sathish Kumar Natarajan, Rodrigo Franco and Hyun-Seob Song
Antioxidants 2022, 11(4), 689; https://doi.org/10.3390/antiox11040689 - 31 Mar 2022
Cited by 11 | Viewed by 4790
Abstract
Arsenic, a naturally occurring metalloid derived from the environment, has been studied worldwide for its causative effects in various cancers. However, the effects of arsenic toxicity on the development and progression of metabolic syndrome, including obesity and diabetes, has received less attention. Many [...] Read more.
Arsenic, a naturally occurring metalloid derived from the environment, has been studied worldwide for its causative effects in various cancers. However, the effects of arsenic toxicity on the development and progression of metabolic syndrome, including obesity and diabetes, has received less attention. Many studies suggest that metabolic dysfunction and autophagy dysregulation of adipose and muscle tissues are closely related to the development of metabolic disease. In the USA, arsenic contamination has been reported in some ground water, soil and grain samples in major agricultural regions, but the effects on adipose and muscle tissue metabolism and autophagy have not been investigated much. Here, we highlight arsenic toxicity according to the species, dose and exposure time and the effects on adipose and muscle tissue metabolism and autophagy. Historically, arsenic was used as both a poison and medicine, depending on the dose and treatment time. In the modern era, arsenic intoxication has significantly increased due to exposure from water, soil and food, which could be a contributing factor in the development and progression of metabolic disease. From this review, a better understanding of the pathogenic mechanisms by which arsenic alters metabolism and autophagy regulation could become a cornerstone leading to the development of therapeutic strategies against arsenic-induced toxicity and metabolic disease. Full article
(This article belongs to the Special Issue Oxidative Stress, Inflammation and Mitochondrial Dysfunction: Mutual Interactions in Obesity-Related Pathologies)
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