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Biomolecules
Special Issues
Mitochondria and Energy Metabolism in Health and Disease
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Mitochondria and Energy Metabolism in Health and Disease

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 5446

Special Issue Editor

Dr. Boris F. Krasnikov

E-Mail Website
Guest Editor
Department of Analysis and Prediction of Medical and Biological Health Risks, Centre for Strategic Planning of FMBA of Russia, Moscow 119121, Russia
Interests: mitochondria; energy metabolism; ageing; nitrogen and sulfur metabolism; bioactivation mechanisms; cancer development

Special Issue Information

Dear Colleagues,

This Special Issue is devoted to the study of the role of mitochondria not only from the point of view of their function in the cell as the main participant in energy metabolism, but also regarding the implementation of their alternative functions, such as participation in apoptosis and cell proliferation, regulation of the redox state of the cell and the second-level messengers, heme and steroid synthesis, detoxification and heat production in health and disease. Despite the fact that a wealth of information regarding these well-coordinated processes in healthy cells has been accumulated, unresolved issues regarding the large-scale functioning of mitochondria and the mechanisms of energy metabolism in various pathologies, such as aging, age-related and other diseases, ranging, but not limited to, from type 2 diabetes and cardiovascular disease, to cancer and neurodegenerative diseases, there is still much left to uncover.

Thus, the purpose of this Special Issue is to take a fresh look at the relationship between energy metabolism and associated processes in the development of pathophysiological mechanisms in the cell. For example, the well-known phenomenon of adaptation of the energy metabolism by transformed cells to maintain tumor initiation and progression (despite the disruption of mitochondrial oxidative metabolism) does not lead to the suppression of mitochondrial functions, but rather to their reprogramming to meet the increased demand for precursors biosynthesis and to mitigate oxidative phosphorylation to limit the production of harmful reactive oxygen species. As a result, specific mitochondrial activity is directed to maintain biological processes that promote tumor growth, invasion, migration, and metastasis.
Understanding how changes in mitochondrial function and energy metabolism contribute to the development and progression of diseases can help in choosing approaches to use mitochondria as targets for the most effective therapy for various diseases.

We invite authors to contribute to this Special Issue with original basic and clinical research on energy metabolism (including studies of the metabolome, proteome, and lipidome as a tool to detect defects in energy metabolism) in health and disease. Meta-analyses and systematic reviews are also highly encouraged. However, reviews should not simply contemplate cited literary sources, but should carry a critical analysis of their own and be the bearer of the original author's idea on the problem considered in the review.

Dr. Boris F. Krasnikov
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
  • energy metabolism
  • metabolomics
  • proteomics
  • lipidomics
  • metabolic diseases
  • aging
  • antitumor therapy
  • tumor progression
  • cell death

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Published Papers (3 papers)

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Research

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23 pages, 2890 KiB  
Article
Energy Metabolites and Indicative Significance of α-Ketoglutarate and α-Ketoglutaramate in Assessing the Progression of Chronic Hepatoencephalopathy
by Yevgeniya I. Shurubor, Andrey B. Krasnikov, Elena P. Isakova, Yulia I. Deryabina, Vladimir S. Yudin, Anton A. Keskinov and Boris F. Krasnikov
Biomolecules 2024, 14(2), 217; https://doi.org/10.3390/biom14020217 - 12 Feb 2024
Viewed by 1313
Abstract
In the example of a rat model with chronic hepatoencephalopathy (HE), changes in the organ morphology of rats affect the balance of metabolites of the tricarboxylic acid (TCA) cycle and metabolites of the glutamine–glutamate (Gln-Glu) cycle, namely α-ketoglutarate (αKG) and α-ketoglutaramate (αKGM), as [...] Read more.
In the example of a rat model with chronic hepatoencephalopathy (HE), changes in the organ morphology of rats affect the balance of metabolites of the tricarboxylic acid (TCA) cycle and metabolites of the glutamine–glutamate (Gln-Glu) cycle, namely α-ketoglutarate (αKG) and α-ketoglutaramate (αKGM), as well as the enzymes associated with them, ω-amidase (ωA) and glutamine transaminase (GTK). This model of rats was obtained as a result of 2–22 weeks of consumption by animals of hepatotoxin thioacetamide (TAA) added to drinking water at a concentration of 0.4 g/L. The control (n = 26) and TAA-induced (n = 55) groups of rats consisted of 11 cohorts each. The control cohorts consisted of 2–4 rats, and the TAA-induced cohorts consisted of 4–7 individuals. Every two weeks, samples of blood plasma, liver, kidney, and brain tissues were taken from the next cohort of rats (a total of 320 samples). By the end of the experiment, irreversible morphological changes were observed in the organs of rats: the weight of the animals was reduced up to ~45%, the weight of the kidneys up to 5%, the brain up to ~20%, and the weight of the liver increased up to ~20%. The analysis revealed: (i) a decrease in the activity of ωA and GTK in the tissues of the brain, kidneys, and liver of rats with chronic HE (by ~3, 40, and 65% and ~10, 60, and 70%, respectively); and (ii) the appearance of a significant imbalance in the content of metabolites of the Gln-Glu cycle, αKG, and αKGM. It is indicative that a ~1.5–12-fold increase in the level of αKG in the blood plasma and tissues of the organs of rats with chronic HE was accompanied by a synchronous, ~1.2–2.5-fold decrease in the level of αKGM. The data obtained indicate an essential involvement of the Gln-Glu cycle in the regulation of energy metabolism in rats under conditions of chronic HE. Attention is focused on the significance of the αKG/αKGM ratio, which can act as a potential marker for diagnosing the degree of HE development. Full article
(This article belongs to the Special Issue Mitochondria and Energy Metabolism in Health and Disease)
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32 pages, 4463 KiB  
Article
Elucidating Events within the Black Box of Enzyme Catalysis in Energy Metabolism: Insights into the Molecular Mechanism of ATP Hydrolysis by F1-ATPase
by Sunil Nath
Biomolecules 2023, 13(11), 1596; https://doi.org/10.3390/biom13111596 - 30 Oct 2023
Cited by 4 | Viewed by 1631
Abstract
Oxygen exchange reactions occurring at β-catalytic sites of the FOF1-ATP synthase/F1-ATPase imprint a unique record of molecular events during the catalytic cycle of ATP synthesis/hydrolysis. This work presents a new theory of oxygen exchange and tests it [...] Read more.
Oxygen exchange reactions occurring at β-catalytic sites of the FOF1-ATP synthase/F1-ATPase imprint a unique record of molecular events during the catalytic cycle of ATP synthesis/hydrolysis. This work presents a new theory of oxygen exchange and tests it on oxygen exchange data recorded on ATP hydrolysis by mitochondrial F1-ATPase (MF1). The apparent rate constant of oxygen exchange governing the intermediate Pi–HOH exchange accompanying ATP hydrolysis is determined by kinetic analysis over a ~50,000-fold range of substrate ATP concentration (0.1–5000 μM) and a corresponding ~200-fold range of reaction velocity (3.5–650 [moles of Pi/{moles of F1-ATPase}−1 s−1]). Isotopomer distributions of [18O]Pi species containing 0, 1, 2, and 3 labeled oxygen atoms predicted by the theory have been quantified and shown to be in perfect agreement with the experimental distributions over the entire range of medium ATP concentrations without employing adjustable parameters. A novel molecular mechanism of steady-state multisite ATP hydrolysis by the F1-ATPase has been proposed. Our results show that steady-state ATP hydrolysis by F1-ATPase occurs with all three sites occupied by Mg-nucleotide. The various implications arising from models of energy coupling in ATP synthesis/hydrolysis by the ATP synthase/F1-ATPase have been discussed. Current models of ATP hydrolysis by F1-ATPase, including those postulated from single-molecule data, are shown to be effectively bisite models that contradict the data. The trisite catalysis formulated by Nath’s torsional mechanism of energy transduction and ATP synthesis/hydrolysis since its first appearance 25 years ago is shown to be in better accord with the experimental record. The total biochemical information on ATP hydrolysis is integrated into a consistent model by the torsional mechanism of ATP synthesis/hydrolysis and shown to elucidate the elementary chemical and mechanical events within the black box of enzyme catalysis in energy metabolism by F1-ATPase. Full article
(This article belongs to the Special Issue Mitochondria and Energy Metabolism in Health and Disease)
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Review

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25 pages, 2578 KiB  
Review
Mitochondria in Multi-Directional Differentiation of Dental-Derived Mesenchymal Stem Cells
by Haotian Liu, Ke Xu, Yifan He and Fang Huang
Biomolecules 2024, 14(1), 12; https://doi.org/10.3390/biom14010012 - 21 Dec 2023
Cited by 2 | Viewed by 2098
Abstract
The pursuit of tissue regeneration has fueled decades of research in regenerative medicine. Among the numerous types of mesenchymal stem cells (MSCs), dental-derived mesenchymal stem cells (DMSCs) have recently emerged as a particularly promising candidate for tissue repair and regeneration. In recent years, [...] Read more.
The pursuit of tissue regeneration has fueled decades of research in regenerative medicine. Among the numerous types of mesenchymal stem cells (MSCs), dental-derived mesenchymal stem cells (DMSCs) have recently emerged as a particularly promising candidate for tissue repair and regeneration. In recent years, evidence has highlighted the pivotal role of mitochondria in directing and orchestrating the differentiation processes of DMSCs. Beyond mitochondrial energy metabolism, the multifaceted functions of mitochondria are governed by the mitochondrial quality control (MQC) system, encompassing biogenesis, autophagy, and dynamics. Notably, mitochondrial energy metabolism not only governs the decision to differentiate but also exerts a substantial influence on the determination of differentiation directions. Furthermore, the MQC system exerts a nuanced impact on the differentiation of DMSCs by finely regulating the quality and mass of mitochondria. The review aims to provide a comprehensive overview of the regulatory mechanisms governing the multi-directional differentiation of DMSCs, mediated by both mitochondrial energy metabolism and the MQC system. We also focus on a new idea based on the analysis of data from many research groups never considered before, namely, DMSC-based regenerative medicine applications. Full article
(This article belongs to the Special Issue Mitochondria and Energy Metabolism in Health and Disease)
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