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Cellular and Molecular Biology of Mitochondria and Oxidative Stress in Human Diseases

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

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 5593

Special Issue Editor

Dr. Kazuo Kobayashi

E-Mail Website
Guest Editor
The Institute of Scientific and Industrial Research, Osaka University, Suita, Japan
Interests: active oxygen; pulse radiolysis; DNA damage; sensor; transcription factor

Special Issue Information

Dear Colleagues,

Mitochondria are the powerhouses of the cell and are involved in essential functions of the cell, including ATP production, intracellular Ca2+ regulation, reactive oxygen species production & scavenging, regulation of apoptotic cell death, and activation of the caspase family of proteases. Mitochondrial dysfunction and oxidative stress are largely involved in aging, cancer, and age-related neurodegenerative and metabolic syndrome. So understanding the mitochondrial structure, function and physiology will help us to develop therapeutic strategies which mainly focused to reduce mitochondrial dysfunction and oxidative stress and maintaining mitochondrial quality in metabolic syndromes.

This Special Issue is devoted to all aspects of mitochondrial function and dysfunction in healthy and diseased cells. It will contain articles that collectively provide a balanced, state-of-the-art view of mitochondrial biology. We seek submissions of high-quality articles including, but not limited to, mitochondrial biogenesis, metabolism, regulation, gene expression, signaling, and roles in aging and disease.

Dr. Kazuo Kobayashi
Guest Editor

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

  • mitochondria
  • mitochondrial biogenesis
  • mitochondrial metabolism
  • mitochondrial gene expression
  • mitochondrial signaling
  • oxidative stress
  • autophagy
  • apoptosis
  • neurodegenerative diseases
  • aging
  • cancer

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Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

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Research

18 pages, 2982 KiB  
Article
Gemfibrozil Improves Microcirculatory Oxygenation of Colon and Liver without Affecting Mitochondrial Function in a Model of Abdominal Sepsis in Rats
by Anne Kuebart, Katharina Gross, Charlotte Maicher, Max Sonnenschein, Annika Raupach, Jan Schulz, Richard Truse, Stefan Hof, Carsten Marcus, Christian Vollmer, Inge Bauer, Olaf Picker, Borna Relja and Anna Herminghaus
Int. J. Mol. Sci. 2024, 25(1), 262; https://doi.org/10.3390/ijms25010262 - 23 Dec 2023
Cited by 1 | Viewed by 1341
Abstract
Recent studies observed, despite an anti-hyperlipidaemic effect, a positive impact of fibrates on septic conditions. This study evaluates the effects of gemfibrozil on microcirculatory variables, mitochondrial function, and lipid peroxidation levels with regard to its potential role as an indicator for oxidative stress [...] Read more.
Recent studies observed, despite an anti-hyperlipidaemic effect, a positive impact of fibrates on septic conditions. This study evaluates the effects of gemfibrozil on microcirculatory variables, mitochondrial function, and lipid peroxidation levels with regard to its potential role as an indicator for oxidative stress in the colon and liver under control and septic conditions and dependencies on PPARα-mediated mechanisms of action. With the approval of the local ethics committee, 120 Wistar rats were randomly divided into 12 groups. Sham and septic animals were treated with a vehicle, gemfibrozil (30 and 100 mg/kg BW), GW 6471 (1 mg/kg BW, PPARα inhibitor), or a combination of both drugs. Sepsis was induced via the colon ascendens stent peritonitis (CASP) model. Then, 24 h post sham or CASP surgery, a re-laparotomy was performed. Measures of vital parameters (heart rate (HR), mean arterial pressure (MAP), and microcirculation (µHbO2)) were recorded for 90 min. Mitochondrial respirometry and assessment of lipid peroxidation via a malondialdehyde (MDA) assay were performed on colon and liver tissues. In the untreated sham animals, microcirculation remained stable, while pre-treatment with gemfibrozil showed significant decreases in the microcirculatory oxygenation of the colon. In the CASP animals, µHbO2 levels in the colon and the liver were significantly decreased 90 min after laparotomy. Pre-treatment with gemfibrozil prevented the microcirculatory aberrations in both organs. Gemfibrozil did not affect mitochondrial function and lipid peroxidation levels in the sham or CASP animals. Gemfibrozil treatment influences microcirculation depending on the underlying condition. Gemfibrozil prevents sepsis-induced microcirculatory aberrances in the colon and liver PPARα-independently. In non-septic animals, gemfibrozil impairs the microcirculatory variables in the colon without affecting those in the liver. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology of Mitochondria and Oxidative Stress in Human Diseases)
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14 pages, 1960 KiB  
Article
Sex-Specific Effects of Prenatal Hypoxia and a Placental Antioxidant Treatment on Cardiac Mitochondrial Function in the Young Adult Offspring
by Paulami Chatterjee, Claudia D. Holody, Raven Kirschenman, Murilo E. Graton, Floor Spaans, Tom J. Phillips, C. Patrick Case, Stephane L. Bourque, Hélène Lemieux and Sandra T. Davidge
Int. J. Mol. Sci. 2023, 24(17), 13624; https://doi.org/10.3390/ijms241713624 - 3 Sep 2023
Cited by 2 | Viewed by 1831
Abstract
Prenatal hypoxia is associated with placental oxidative stress, leading to impaired fetal growth and an increased risk of cardiovascular disease in the adult offspring; however, the mechanisms are unknown. Alterations in mitochondrial function may result in impaired cardiac function in offspring. In this [...] Read more.
Prenatal hypoxia is associated with placental oxidative stress, leading to impaired fetal growth and an increased risk of cardiovascular disease in the adult offspring; however, the mechanisms are unknown. Alterations in mitochondrial function may result in impaired cardiac function in offspring. In this study, we hypothesized that cardiac mitochondrial function is impaired in adult offspring exposed to intrauterine hypoxia, which can be prevented by placental treatment with a nanoparticle-encapsulated mitochondrial antioxidant (nMitoQ). Cardiac mitochondrial respiration was assessed in 4-month-old rat offspring exposed to prenatal hypoxia (11% O2) from gestational day (GD)15–21 receiving either saline or nMitoQ on GD 15. Prenatal hypoxia did not alter cardiac mitochondrial oxidative phosphorylation capacity in the male offspring. In females, the NADH + succinate pathway capacity decreased by prenatal hypoxia and tended to be increased by nMitoQ. Prenatal hypoxia also decreased the succinate pathway capacity in females. nMitoQ treatment increased respiratory coupling efficiency in prenatal hypoxia-exposed female offspring. In conclusion, prenatal hypoxia impaired cardiac mitochondrial function in adult female offspring only, which was improved with prenatal nMitoQ treatment. Therefore, treatment strategies targeting placental oxidative stress in prenatal hypoxia may reduce the risk of cardiovascular disease in adult offspring by improving cardiac mitochondrial function in a sex-specific manner. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology of Mitochondria and Oxidative Stress in Human Diseases)
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12 pages, 2044 KiB  
Article
A Pacific Oyster-Derived Antioxidant, DHMBA, Protects Renal Tubular HK-2 Cells against Oxidative Stress via Reduction of Mitochondrial ROS Production and Fragmentation
by Hsin-Jung Ho, Natsumi Aoki, Yi-Jou Wu, Ming-Chen Gao, Karin Sekine, Toshihiro Sakurai, Hitoshi Chiba, Hideaki Watanabe, Mitsugu Watanabe and Shu-Ping Hui
Int. J. Mol. Sci. 2023, 24(12), 10061; https://doi.org/10.3390/ijms241210061 - 13 Jun 2023
Cited by 5 | Viewed by 1776
Abstract
The kidney contains numerous mitochondria in proximal tubular cells that provide energy for tubular secretion and reabsorption. Mitochondrial injury and consequent excessive reactive oxygen species (ROS) production can cause tubular damage and play a major role in the pathogenesis of kidney diseases, including [...] Read more.
The kidney contains numerous mitochondria in proximal tubular cells that provide energy for tubular secretion and reabsorption. Mitochondrial injury and consequent excessive reactive oxygen species (ROS) production can cause tubular damage and play a major role in the pathogenesis of kidney diseases, including diabetic nephropathy. Accordingly, bioactive compounds that protect the renal tubular mitochondria from ROS are desirable. Here, we aimed to report 3,5-dihydroxy-4-methoxybenzyl alcohol (DHMBA), isolated from the Pacific oyster (Crassostrea gigas) as a potentially useful compound. In human renal tubular HK-2 cells, DHMBA significantly mitigated the cytotoxicity induced by the ROS inducer L-buthionine-(S, R)-sulfoximine (BSO). DHMBA reduced the mitochondrial ROS production and subsequently regulated mitochondrial homeostasis, including mitochondrial biogenesis, fusion/fission balance, and mitophagy; DHMBA also enhanced mitochondrial respiration in BSO-treated cells. These findings highlight the potential of DHMBA to protect renal tubular mitochondrial function against oxidative stress. Full article
(This article belongs to the Special Issue Cellular and Molecular Biology of Mitochondria and Oxidative Stress in Human Diseases)
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