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Genes
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Alterations in mtDNA and Mitochondrial Quality Control
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Alterations in mtDNA and Mitochondrial Quality Control

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 July 2021) | Viewed by 18471

Special Issue Editors

Dr. Angela Maria Serena Lezza

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Guest Editor
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70125 Bari, Italy
Interests: aging; mitochondrial biogenesis in aging; mitochondrial pathologies; pathologies with mitochondrial oxidative stress (age-related diseases, autoimmune and inflammatory pathologies, neurodegenerative diseases); calorie restriction and nutritional anti-aging interventions; mtDNA–TFAM relationships
Special Issues, Collections and Topics in MDPI journals
Dr. Vito Pesce

E-Mail Website
Guest Editor
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70125 Bari, Italy
Interests: mtDNA damage and deletions; mitochondrial oxidative stress and antioxidant defense; mitochondrial biogenesis and dynamics; mitochondrial quality control; mitochondrial dysfunction in aging and age-related degenerative disorders; nutritional anti-aging interventions
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Guglielmina Chimienti

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Guest Editor
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, 70125 Bari, Italy
Interests: interplay between inflammation and oxidative stress; nutritional interventions; qualitative and quantitative alterations of mtDNA; mitochondrial biogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria have their own DNA (mtDNA) that can be damaged by endogenous and exogenous agents, leading to the appearance of various types of genetic alterations (mutations, abasic sites, double-strand and single-strand breaks, modified bases) that can compromise, at different levels, the organelle’s functionality. To prevent such a dangerous cascade, several quality control processes, including mtDNA repair and replication, mitochondrial dynamics, and mitophagy, have been developed. Knowledge of this large array of quality control processes is constantly growing as progressive studies unveil their reciprocal and tight relationships together with the pathologies arising from defects in any of them. Therefore, restoration of impaired quality control processes or enhancement of not anymore adequate ones constitute the most recent and alternative therapeutic strategy for otherwise untreatable diseases.

The goal of this Special Issue, dedicated to “Alterations in mtDNA and Mitochondrial Quality Control”, is to provide a broad and updated overview of this fast-moving field that might allow useful comparisons and be inspiring for future developments. Therefore, contributions by experts of the field in the form of research papers and critical reviews are called for.

Prof. Dr. Angela Maria Serena Lezza
Prof. Dr. Vito Pesce
Prof. Dr. Guglielmina Chimienti
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. Genes 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

  • Mitochondrial DNA alterations
  • Mitochondrial quality control
  • Pathologies related to impaired mitochondrial quality control
  • Mitochondrial DNA repair
  • Mitochondrial dynamics
  • Therapeutic strategies targeting defective mitochondrial quality control mechanisms

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Published Papers (4 papers)

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Research

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13 pages, 1067 KiB  
Article
The Mitochondrial Trigger in an Animal Model of Nonalcoholic Fatty Liver Disease
by Guglielmina Chimienti, Antonella Orlando, Francesco Russo, Benedetta D’Attoma, Manuela Aragno, Eleonora Aimaretti, Angela Maria Serena Lezza and Vito Pesce
Genes 2021, 12(9), 1439; https://doi.org/10.3390/genes12091439 - 18 Sep 2021
Cited by 13 | Viewed by 2850
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the leading liver chronic disease featuring hepatic steatosis. Mitochondrial β-oxidation participates in the derangement of lipid metabolism at the basis of NAFLD, and mitochondrial oxidative stress contributes to the onset of the disease. We evaluated the presence [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) is the leading liver chronic disease featuring hepatic steatosis. Mitochondrial β-oxidation participates in the derangement of lipid metabolism at the basis of NAFLD, and mitochondrial oxidative stress contributes to the onset of the disease. We evaluated the presence and effects of mitochondrial oxidative stress in the liver from rats fed a high-fat plus fructose (HF-F) diet inducing NAFLD. Supplementation with dehydroepiandrosterone (DHEA), a multitarget antioxidant, was tested for efficacy in delaying NAFLD. A marked mitochondrial oxidative stress was originated by all diets, as demonstrated by the decrease in Superoxide Dismutase 2 (SOD2) and Peroxiredoxin III (PrxIII) amounts. All diets induced a decrease in mitochondrial DNA content and an increase in its oxidative damage. The diets negatively affected mitochondrial biogenesis as shown by decreased peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α), mitochondrial transcription factor A (TFAM), and the COX-IV subunit from the cytochrome c oxidase complex. The reduced amounts of Beclin-1 and lipidated LC3 II form of the microtubule-associated protein 1 light chain 3 (LC3) unveiled the diet-related autophagy’s decrease. The DHEA supplementation did not prevent the diet-induced changes. These results demonstrate the relevance of mitochondrial oxidative stress and the sequential dysfunction of the organelles in an obesogenic diet animal model of NAFLD. Full article
(This article belongs to the Special Issue Alterations in mtDNA and Mitochondrial Quality Control)
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Review

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14 pages, 1582 KiB  
Review
Mitochondrial Dysfunction in Diseases, Longevity, and Treatment Resistance: Tuning Mitochondria Function as a Therapeutic Strategy
by Kazuo Tomita, Yoshikazu Kuwahara, Kento Igarashi, Mehryar Habibi Roudkenar, Amaneh Mohammadi Roushandeh, Akihiro Kurimasa and Tomoaki Sato
Genes 2021, 12(9), 1348; https://doi.org/10.3390/genes12091348 - 29 Aug 2021
Cited by 13 | Viewed by 5413
Abstract
Mitochondria are very important intracellular organelles because they have various functions. They produce ATP, are involved in cell signaling and cell death, and are a major source of reactive oxygen species (ROS). Mitochondria have their own DNA (mtDNA) and mutation of mtDNA or [...] Read more.
Mitochondria are very important intracellular organelles because they have various functions. They produce ATP, are involved in cell signaling and cell death, and are a major source of reactive oxygen species (ROS). Mitochondria have their own DNA (mtDNA) and mutation of mtDNA or change the mtDNA copy numbers leads to disease, cancer chemo/radioresistance and aging including longevity. In this review, we discuss the mtDNA mutation, mitochondrial disease, longevity, and importance of mitochondrial dysfunction in cancer first. In the later part, we particularly focus on the role in cancer resistance and the mitochondrial condition such as mtDNA copy number, mitochondrial membrane potential, ROS levels, and ATP production. We suggest a therapeutic strategy employing mitochondrial transplantation (mtTP) for treatment-resistant cancer. Full article
(This article belongs to the Special Issue Alterations in mtDNA and Mitochondrial Quality Control)
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13 pages, 1141 KiB  
Review
Interactions of Mitochondrial Transcription Factor A with DNA Damage: Mechanistic Insights and Functional Implications
by Krystie Chew and Linlin Zhao
Genes 2021, 12(8), 1246; https://doi.org/10.3390/genes12081246 - 15 Aug 2021
Cited by 17 | Viewed by 4068
Abstract
Mitochondria have a plethora of functions in eukaryotic cells, including cell signaling, programmed cell death, protein cofactor synthesis, and various aspects of metabolism. The organelles carry their own genomic DNA, which encodes transfer and ribosomal RNAs and crucial protein subunits in the oxidative [...] Read more.
Mitochondria have a plethora of functions in eukaryotic cells, including cell signaling, programmed cell death, protein cofactor synthesis, and various aspects of metabolism. The organelles carry their own genomic DNA, which encodes transfer and ribosomal RNAs and crucial protein subunits in the oxidative phosphorylation system. Mitochondria are vital for cellular and organismal functions, and alterations of mitochondrial DNA (mtDNA) have been linked to mitochondrial disorders and common human diseases. As such, how the cell maintains the integrity of the mitochondrial genome is an important area of study. Interactions of mitochondrial proteins with mtDNA damage are critically important for repairing, regulating, and signaling mtDNA damage. Mitochondrial transcription factor A (TFAM) is a key player in mtDNA transcription, packaging, and maintenance. Due to the extensive contact of TFAM with mtDNA, it is likely to encounter many types of mtDNA damage and secondary structures. This review summarizes recent research on the interaction of human TFAM with different forms of non-canonical DNA structures and discusses the implications on mtDNA repair and packaging. Full article
(This article belongs to the Special Issue Alterations in mtDNA and Mitochondrial Quality Control)
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24 pages, 989 KiB  
Review
Mitochondrial Dynamics: Molecular Mechanisms, Related Primary Mitochondrial Disorders and Therapeutic Approaches
by Michela Di Nottia, Daniela Verrigni, Alessandra Torraco, Teresa Rizza, Enrico Bertini and Rosalba Carrozzo
Genes 2021, 12(2), 247; https://doi.org/10.3390/genes12020247 - 10 Feb 2021
Cited by 28 | Viewed by 5267
Abstract
Mitochondria do not exist as individual entities in the cell—conversely, they constitute an interconnected community governed by the constant and opposite process of fission and fusion. The mitochondrial fission leads to the formation of smaller mitochondria, promoting the biogenesis of new organelles. On [...] Read more.
Mitochondria do not exist as individual entities in the cell—conversely, they constitute an interconnected community governed by the constant and opposite process of fission and fusion. The mitochondrial fission leads to the formation of smaller mitochondria, promoting the biogenesis of new organelles. On the other hand, following the fusion process, mitochondria appear as longer and interconnected tubules, which enhance the communication with other organelles. Both fission and fusion are carried out by a small number of highly conserved guanosine triphosphatase proteins and their interactors. Disruption of this equilibrium has been associated with several pathological conditions, ranging from cancer to neurodegeneration, and mutations in genes involved in mitochondrial fission and fusion have been reported to be the cause of a subset of neurogenetic disorders. Full article
(This article belongs to the Special Issue Alterations in mtDNA and Mitochondrial Quality Control)
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