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Biomedicines
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10th Anniversary of Biomedicines—Mitochondrial Biology
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10th Anniversary of Biomedicines—Mitochondrial Biology

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

Deadline for manuscript submissions: closed (15 December 2023) | Viewed by 6903

Special Issue Editor

Dr. Marie-Pierre Golinelli-Cohen

E-Mail Website
Guest Editor
Institut de Chimie des Substances Naturelles, CNRS Centre National de la Recherche Scientifique, Gif-sur-Yvette, France
Interests: Fe-S proteins; Fe-S cluster biogenesis; protein structure and function; oxidative stress; cell fate
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The year 2023 marks the 10th anniversary of Biomedicines, a peer-reviewed, open-access journal in the biomedical field. So far, Biomedicines has published more than 2700 papers from more than 17,000 authors. We appreciate each author, reviewer, and academic editor whose support has brought us to where we are today.

To celebrate this significant milestone, we aim to publish a Special Issue entitled “10th Anniversary of Biomedicines—Mitochondrial Biology”. This mitochondrion is well known as the powerhouse of the eukaryotic cell, but it also plays a pivotal role in the regulation of signaling pathways, and in cell differentiation, proliferation and death. Thus, mitochondrial dysfunction is linked to numerous human pathologies, ranging from rare diseases to diseases with a very high societal impact (e.g., cancer, neurodegenerative diseases). A better understanding of the mitochondrial function in normal and pathological states is crucial for an improved management of these diseases and for the development of innovative therapies.

This Special Issue focuses on mitochondrial biology, aiming to collect submissions of original research articles or review articles describing the current state of the art of the field.

Dr. Marie-Pierre Golinelli-Cohen
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
  • mitochondrial pathologies
  • mitochondrial diseases
  • signaling
  • metabolism
  • bioenergetics

Published Papers (3 papers)

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Research

16 pages, 3875 KiB  
Article
Chagas Disease Megaesophagus Patients Carrying Variant MRPS18B P260A Display Nitro-Oxidative Stress and Mitochondrial Dysfunction in Response to IFN-γ Stimulus
by Karla Deysiree Alcântara Silva, João Paulo Silva Nunes, Pauline Andrieux, Pauline Brochet, Rafael Ribeiro Almeida, Andréia Cristina Kazue Kuramoto Takara, Natalia Bueno Pereira, Laurent Abel, Aurelie Cobat, Ricardo Costa Fernandes Zaniratto, Débora Levy, Sergio Paulo Bydlowski, Ivan Cecconello, Francisco Carlos Bernal da Costa Seguro, Jorge Kalil, Christophe Chevillard and Edecio Cunha-Neto
Biomedicines 2022, 10(9), 2215; https://doi.org/10.3390/biomedicines10092215 - 7 Sep 2022
Cited by 2 | Viewed by 1758
Abstract
Chagas disease (CD), caused by the protozoan parasite Trypanosoma cruzi, affects 8 million people, and around 1/3 develop chronic cardiac (CCC) or digestive disease (megaesophagus/megacolon), while the majority remain asymptomatic, in the indeterminate form of Chagas disease (ASY). Most CCC cases in [...] Read more.
Chagas disease (CD), caused by the protozoan parasite Trypanosoma cruzi, affects 8 million people, and around 1/3 develop chronic cardiac (CCC) or digestive disease (megaesophagus/megacolon), while the majority remain asymptomatic, in the indeterminate form of Chagas disease (ASY). Most CCC cases in families with multiple Chagas disease patients carry damaging mutations in mitochondrial genes. We searched for exonic mutations associated to chagasic megaesophagus (CME) in genes essential to mitochondrial processes. We performed whole exome sequencing of 13 CME and 45 ASY patients. We found the damaging variant MRPS18B 688C > G P230A, in five out of the 13 CME patients (one of them being homozygous; 38.4%), while the variant appeared in one out of 45 ASY patients (2.2%). We analyzed the interferon (IFN)-γ-induced nitro-oxidative stress and mitochondrial function of EBV-transformed lymphoblastoid cell lines. We found the CME carriers of the mutation displayed increased levels of nitrite and nitrated proteins; in addition, the homozygous (G/G) CME patient also showed increased mitochondrial superoxide and reduced levels of ATP production. The results suggest that pathogenic mitochondrial mutations may contribute to cytokine-induced nitro-oxidative stress and mitochondrial dysfunction. We hypothesize that, in mutation carriers, IFN-γ produced in the esophageal myenteric plexus might cause nitro-oxidative stress and mitochondrial dysfunction in neurons, contributing to megaesophagus. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Mitochondrial Biology)
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17 pages, 1619 KiB  
Article
Long-Term Persistence of Mitochondrial DNA Instability in HIV-Exposed Uninfected Children during and after Exposure to Antiretroviral Drugs and HIV
by Valérie Desquiret-Dumas, Morgana D’Ottavi, Audrey Monnin, David Goudenège, Nicolas Méda, Amélie Vizeneux, Chipepo Kankasa, Thorkild Tylleskar, Céline Bris, Vincent Procaccio, Nicolas Nagot, Philippe Van de Perre, Pascal Reynier and Jean-Pierre Molès
Biomedicines 2022, 10(8), 1786; https://doi.org/10.3390/biomedicines10081786 - 25 Jul 2022
Cited by 2 | Viewed by 1638
Abstract
HIV-exposed uninfected (HEU) children show impaired health outcomes during childhood. A high rate of mitochondrial DNA (mtDNA) instability was reported in the blood of HEU at birth. We aimed to explore the relationship between these health outcomes and mtDNA deletions over time in [...] Read more.
HIV-exposed uninfected (HEU) children show impaired health outcomes during childhood. A high rate of mitochondrial DNA (mtDNA) instability was reported in the blood of HEU at birth. We aimed to explore the relationship between these health outcomes and mtDNA deletions over time in a case series of 24 HEU children. MtDNA instability was assessed by deep sequencing and analyzed by eKLIPse-v2 algorithm at three time points, namely birth, 1 year, and 6 years of age. Association between mtDNA deletion and health outcomes, including growth, clinical, and neurodevelopmental parameters, were explored using univariate statistical analyses and after stratification with relevant variables. HEU children were selected with an equal male:female ratio. An elevated number of mtDNA deletions and duplications events was observed at 7 days’ post-partum. Median heteroplasmy increased at one year of life and then returned to baseline by six years of age. The mtDNA instability was acquired and was not transmitted by the mother. No risk factors were significantly associated with mtDNA instability. In this small case series, we did not detect any association between any health outcome at 6 years and mtDNA instability measures. A significant effect modification of the association between the duration of maternal prophylaxis and child growth was observed after stratification with heteroplasmy rate. Genomic instability persists over time among HEU children but, despite its extension, stays subclinical at six years. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Mitochondrial Biology)
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14 pages, 1184 KiB  
Article
Robustness of the Krebs Cycle under Physiological Conditions and in Cancer: New Clues for Evaluating Metabolism-Modifying Drug Therapies
by Rafael Franco and Joan Serrano-Marín
Biomedicines 2022, 10(5), 1199; https://doi.org/10.3390/biomedicines10051199 - 22 May 2022
Cited by 3 | Viewed by 2494
Abstract
The Krebs cycle in cells that contain mitochondria is necessary for both energy production and anabolic processes. In given cell/condition, the Krebs cycle is dynamic but remains at a steady state. In this article, we first aimed at comparing the properties of a [...] Read more.
The Krebs cycle in cells that contain mitochondria is necessary for both energy production and anabolic processes. In given cell/condition, the Krebs cycle is dynamic but remains at a steady state. In this article, we first aimed at comparing the properties of a closed cycle versus the same metabolism in a linear array. The main finding is that, unlike a linear metabolism, the closed cycle can reach a steady state (SS) regardless of the nature and magnitude of the disturbance. When the cycle is modeled with input and output reactions, the “open” cycle is robust and reaches a steady state but with exceptions that lead to sustained accumulation of intermediate metabolites, i.e., conditions at which no SS can be achieved. The modeling of the cycle in cancer, trying to obtain marked reductions in flux, shows that these reductions are limited and therefore the Warburg effect is moderate at most. In general, our results of modeling the cycle in different conditions and looking for the achievement, or not, of SS, suggest that the cycle may have a regulation, not yet discovered, to go from an open cycle to a closed one. Said regulation could allow for reaching the steady state, thus avoiding the unwanted effects derived from the aberrant accumulation of metabolites in the mitochondria. The information in this paper might be useful to evaluate metabolism-modifying medicines. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Mitochondrial Biology)
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