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Biomolecules
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Animal Models: Explore the Oxidative Stress Accumulation, Mitochondrial Dysfunction, and...
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Animal Models: Explore the Oxidative Stress Accumulation, Mitochondrial Dysfunction, and Aging Mechanism

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 4205

Special Issue Editor

Prof. Dr. Yoshihiro H. Inoue

E-Mail Website
Guest Editor
Biomedical Research Center, Kyoto Institute of Technology, Matsugasaki, Kyoto 606-0962, Sakyo, Japan
Interests: Drosophila; development; DNA repair; oxidative stress; aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The hypothesis that Reactive Oxygen Spices (ROS), containing free radicals generated in living organisms, contribute to aging progression have been proposed. As most of intracellular ROS is produced in mitochondria, it is important to understand how the mtDNA and proteins in the organelles are damaged, and they contribute aging progression. The mtDNA damages impair the translational capacity and, consequently, this results in insufficient protein supply in the organelle. Thereby, the increased levels of ROS can results in a vicious cycle that generates further mtDNA damages. However, further investigation using animal models need to be performed before the conclusion concerning the oxidative stress, mitochondrial dysfunction and ageing. Some recent studies reported the aging-related phenotypes seen in artificial conditions have not always observed in normal aging. Once oxidative damages are accumulated in a mitochondrion, the damaged parts are separated by fission and subsequently removed by mitophagy. It still remains to be studied how mitochondrial dynamics and mitophagy influences aging-related phenomena in animal models. Therefore, we planned to make a Special Issue entitled “Animal Models: Explore the Oxidative Stress Accumulation, Mitochondrial Dysfunction, and Aging Mechanism”. The Special Issue will accept original studies and reviews that deal with these issues using mice, zebrafish, Drosophila, and C. elegans.

Prof. Dr. Yoshihiro H. Inoue
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. Biomolecules 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 2700 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

  • mitochondria dysfunction
  • animal models for human aging-related diseases
  • oxidative stress
  • mitochondria DNA damage
  • aging phenotypes
  • mitophagy
  • apoptosis

Published Papers (2 papers)

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Research

17 pages, 2255 KiB  
Article
Monoamine Oxidase A Contributes to Serotonin—But Not Norepinephrine-Dependent Damage of Rat Ventricular Myocytes
by Jonas Knittel, Nadja Itani, Rolf Schreckenberg, Jacqueline Heger, Susanne Rohrbach, Rainer Schulz and Klaus-Dieter Schlüter
Biomolecules 2023, 13(6), 1013; https://doi.org/10.3390/biom13061013 - 19 Jun 2023
Cited by 1 | Viewed by 1655
Abstract
Serotonin effects on cardiac hypertrophy, senescence, and failure are dependent either on activation of specific receptors or serotonin uptake and serotonin degradation by monoamine oxidases (MAOs). Receptor-dependent effects are specific for serotonin, but MAO-dependent effects are nonspecific as MAOs also metabolize other substrates [...] Read more.
Serotonin effects on cardiac hypertrophy, senescence, and failure are dependent either on activation of specific receptors or serotonin uptake and serotonin degradation by monoamine oxidases (MAOs). Receptor-dependent effects are specific for serotonin, but MAO-dependent effects are nonspecific as MAOs also metabolize other substrates such as catecholamines. Our study evaluates the role of MAO-A in serotonin- and norepinephrine-dependent cell damage. Experiments were performed in vivo to study the regulation of MAOA and MAOB expression and in vitro on isolated cultured adult rat ventricular cardiomyocytes (cultured for 24 h) to study the function of MAO-A. MAOA but not MAOB expression increased in maladaptive hypertrophic stages. Serotonin and norepinephrine induced morphologic cell damage (loss of rod-shaped cell structure). However, MAO-A inhibition suppressed serotonin-dependent but not norepinephrine-dependent damages. Serotonin but not norepinephrine caused a reduction in cell shortening in nondamaged cells. Serotonin induced mitochondria-dependent oxidative stress. In vivo, MAOA was induced during aging and hypertension but the expression of the corresponding serotonin uptake receptor (SLC6A4) was reduced and enzymes that reduce either oxidative stress (CAT) or accumulation of 5-hydroxyindolacetaldehyde (ALDH2) were induced. In summary, the data show that MAO-A potentially affects cardiomyocytes’ function but that serotonin is not necessarily the native substrate. Full article
(This article belongs to the Special Issue Animal Models: Explore the Oxidative Stress Accumulation, Mitochondrial Dysfunction, and Aging Mechanism)
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22 pages, 23317 KiB  
Article
Downregulating Mitochondrial DNA Polymerase γ in the Muscle Stimulated Autophagy, Apoptosis, and Muscle Aging-Related Phenotypes in Drosophila Adults
by Mika Ozaki, Tuan Dat Le and Yoshihiro H. Inoue
Biomolecules 2022, 12(8), 1105; https://doi.org/10.3390/biom12081105 - 11 Aug 2022
Cited by 1 | Viewed by 2135
Abstract
Reactive oxygen species, generated as by-products of mitochondrial electron transport, can induce damage to mitochondrial DNA (mtDNA) and proteins. Here, we investigated whether the moderate accumulation of mtDNA damage in adult muscles resulted in accelerated aging-related phenotypes in Drosophila. DNA polymerase γ [...] Read more.
Reactive oxygen species, generated as by-products of mitochondrial electron transport, can induce damage to mitochondrial DNA (mtDNA) and proteins. Here, we investigated whether the moderate accumulation of mtDNA damage in adult muscles resulted in accelerated aging-related phenotypes in Drosophila. DNA polymerase γ (Polγ) is the sole mitochondrial DNA polymerase. The muscle-specific silencing of the genes encoding the polymerase subunits resulted in the partial accumulation of mtDNA with oxidative damage and a reduction in the mtDNA copy number. This subsequently resulted in the production of abnormal mitochondria with reduced membrane potential and, consequently, a partially reduced ATP quantity in the adult muscle. Immunostaining indicated a moderate increase in autophagy and mitophagy in adults with RNA interference of Polγ (PolγRNAi) muscle cells with abnormal mitochondria. In adult muscles showing continuous silencing of Polγ, malformation of both myofibrils and mitochondria was frequently observed. This was associated with the partially enhanced activation of pro-apoptotic caspases in the muscle. Adults with muscle-specific PolγRNAi exhibited a shortened lifespan, accelerated age-dependent impairment of locomotor activity, and disturbed circadian rhythms. Our findings in this Drosophila model contribute to understanding how the accumulation of mtDNA damage results in impaired mitochondrial activity and how this contributes to muscle aging. Full article
(This article belongs to the Special Issue Animal Models: Explore the Oxidative Stress Accumulation, Mitochondrial Dysfunction, and Aging Mechanism)
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