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Biomedicines
Special Issues
Mitochondrial Dysfunction and Oxidative Stress in Aging and Disease 2.0
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Mitochondrial Dysfunction and Oxidative Stress in Aging and Disease 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 4704

Special Issue Editor

Dr. Chia-Jung Li

E-Mail Website
Guest Editor
Department of Obstetrics and Gynecology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan
Interests: mitochondrial medicine; free radical biology; reproduction; cancer biology; chronic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are considered to have a significant influence on aging due to their critical role in the regulation of bioenergetics, oxidative stress, and cell death. Mitochondrial oxidative stress, commonly associated with age-related pathologies (neurodegenerative syndromes, cardiovascular diseases, endocrine pathologies, diabetes, and cancer), leads to damage to mitochondrial DNA, proteins, and lipids. The increased ROS presence can also induce chronic inflammation, which often characterizes age-related diseases and autoimmune pathologies. Therefore, it is important to understand the molecular mechanisms, both those which are established as well as novel mechanisms, and how these mechanisms affect the antioxidant process—particularly how they protect cells and organs from the harmful effects of free radicals to successfully carry out metabolic processes and eliminate disease. Of particular interest is how these mechanisms protect cells and organs from the harmful effects of free radicals for disease treatment. A better understanding of mitochondrial dysfunction and oxidative stress will lead to new treatments to prevent or improve age-related degenerative diseases. This Special Issue aims to provide a broad and updated overview of the involvement of “Mitochondrial dysfunction and oxidative stress in aging and disease” with the hope of shedding light on model systems, diagnostic biomarkers, pathophysiological mechanisms, and novel therapeutic approaches. To advance the knowledge of these intricate issues, we call for contributions from experts in the field in the form of research papers and critical reviews.

Dr. Chia-Jung Li
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. Biomedicines 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 2600 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
  • ROS
  • aging
  • longevity
  • healthspan
  • pathology
  • antioxidant
  • age-related disease

Published Papers (3 papers)

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Research

13 pages, 2908 KiB  
Article
Measuring Mitochondrial Oxygen Tension during Red Blood Cell Transfusion in Chronic Anemia Patients: A Pilot Study
by Rinse Ubbink, Lucia W. J. M. Streng, Nicolaas J. H. Raat, Floor A. Harms, Peter A. W. te Boekhorst, Robert J. Stolker and Egbert G. Mik
Biomedicines 2023, 11(7), 1873; https://doi.org/10.3390/biomedicines11071873 - 30 Jun 2023
Cited by 1 | Viewed by 837
Abstract
In light of the associated risks, the question has been raised whether the decision to give a blood transfusion should solely be based on the hemoglobin level. As mitochondria are the final destination of oxygen transport, mitochondrial parameters are suggested to be of [...] Read more.
In light of the associated risks, the question has been raised whether the decision to give a blood transfusion should solely be based on the hemoglobin level. As mitochondria are the final destination of oxygen transport, mitochondrial parameters are suggested to be of added value. The aims of this pilot study were to investigate the effect of a red blood cell transfusion on mitochondrial oxygenation as measured by the COMET device in chronic anemia patients and to explore the clinical usability of the COMET monitor in blood transfusion treatments, especially the feasibility of performing measurements in an outpatient setting. To correct the effect of volume load on mitochondrial oxygenation, a red blood cell transfusion and a saline infusion were given in random order. In total, 21 patients were included, and this resulted in 31 observations. If patients participated twice, the order of infusion was reversed. In both the measurements wherein a blood transfusion was given first and wherein 500 mL of 0.9% saline was given first, the median mitochondrial oxygen tension decreased after red blood cell transfusion. The results of this study have strengthened the need for further research into the effect of blood transfusion tissue oxygenation and the potential role of mitochondrial parameters herein. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Aging and Disease 2.0)
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15 pages, 303 KiB  
Article
Mitochondrial DNA Changes in Respiratory Complex I Genes in Brain Gliomas
by Paulina Kozakiewicz, Ludmiła Grzybowska-Szatkowska, Marzanna Ciesielka, Paulina Całka, Jacek Osuchowski, Paweł Szmygin, Bożena Jarosz, Marta Ostrowska-Leśko, Jarosław Dudka, Angelika Tkaczyk-Wlizło and Brygida Ślaska
Biomedicines 2023, 11(4), 1183; https://doi.org/10.3390/biomedicines11041183 - 15 Apr 2023
Cited by 1 | Viewed by 1499
Abstract
Mitochondria are organelles necessary for oxidative phosphorylation. The interest in the role of mitochondria in the process of carcinogenesis results from the fact that a respiratory deficit is found in dividing cells, especially in cells with accelerated proliferation. The study included tumor and [...] Read more.
Mitochondria are organelles necessary for oxidative phosphorylation. The interest in the role of mitochondria in the process of carcinogenesis results from the fact that a respiratory deficit is found in dividing cells, especially in cells with accelerated proliferation. The study included tumor and blood material from 30 patients diagnosed with glioma grade II, III and IV according to WHO (World Health Organization). DNA was isolated from the collected material and next-generation sequencing was performed on the MiSeqFGx apparatus (Illumina). The study searched for a possible relationship between the occurrence of specific mitochondrial DNA polymorphisms in the respiratory complex I genes and brain gliomas of grade II, III and IV. The impact of missense changes on the biochemical properties, structure and functioning of the encoded protein, as well as their potential harmfulness, were assessed in silico along with their belonging to a given mitochondrial subgroup. The A3505G, C3992T, A4024G, T4216C, G5046A, G7444A, T11253C, G12406A and G13604C polymorphisms were assessed as deleterious changes in silico, indicating their association with carcinogenesis. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Aging and Disease 2.0)
11 pages, 2230 KiB  
Article
Mitochondrial Transplantation Moderately Ameliorates Retinal Degeneration in Royal College of Surgeons Rats
by Shih-Fang Wu, Chih-Yao Lin, Rong-Kung Tsai, Yao-Tseng Wen, Feng-Huei Lin, Chia-Yu Chang, Ching-I Shen, Shinn-Zong Lin, Horng-Jyh Harn, Tzyy-Wen Chiou, Chin-San Liu, Yan-Ting Chen and Hong-Lin Su
Biomedicines 2022, 10(11), 2883; https://doi.org/10.3390/biomedicines10112883 - 10 Nov 2022
Cited by 1 | Viewed by 1737
Abstract
Retinal pigmented epithelial (RPE) cells possess high mitochondria content for energy production, which is required for phagocytosis and vision cycle metabolism. The mitochondrial integrity in RPE cells helps the homeostasis of photoreceptor turnover and prevents retina aging and degeneration. Mitochondrial transplantation benefits the [...] Read more.
Retinal pigmented epithelial (RPE) cells possess high mitochondria content for energy production, which is required for phagocytosis and vision cycle metabolism. The mitochondrial integrity in RPE cells helps the homeostasis of photoreceptor turnover and prevents retina aging and degeneration. Mitochondrial transplantation benefits the recovery of several acute inflammatory diseases, leading us to investigate the effects of mitochondrial transplantation on retina degeneration. Allogeneic mitochondria were isolated and delivered into the vitreous chamber in the Royal College of Surgeons (RCS) rats, which exhibit inherited and early-onset retina degeneration. The progress of retina degeneration was examined with optical coherence tomography (OCT) and visual evoked potential (VEP) to determine the retina thickness and integrity of afferent electrical signals from affected eyes, respectively. We found that mitochondria engraftment moderately attenuated the degeneration of retinal layers in RCS rats by histological examination. This result was consistent with the OCT measurement of retina thickness around the optic disc. The VEP analysis revealed that the peak one (N1) latency, representing the arriving time of electrical impulse from the retina to cortex, was substantially maintained as the normal value after the mitochondrial transplantation. This result suggests that the intra-vitreous transplanted mitochondria ameliorate the degeneration of photoreceptors in RCS rats and might be potential for clinical application. Full article
(This article belongs to the Special Issue Mitochondrial Dysfunction and Oxidative Stress in Aging and Disease 2.0)
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