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Biomedicines
Special Issues
Mitochondrial Metabolism in Health and Disease
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Mitochondrial Metabolism in Health and Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 14743

Special Issue Editors

Dr. Simona Todisco

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Guest Editor
Department of Sciences, University of Basilicata, Potenza, Italy
Interests: cell metabolism and mitochondrial metabolism; mitochondrial bioenergetics; redox alteration; enzymatic activity; inflammatory response and immunometabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Vittoria Infantino

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Guest Editor
Department of Science, University of Basilicata, Potenza, Italy
Interests: macrophage activation; cell signaling; immunometabolism; gene expression; transcriptional regulation; mitochondria; epigenetic mechanisms
Special Issues, Collections and Topics in MDPI journals
Dr. Paolo Convertini

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Guest Editor
Department of Science, University of Basilicata, Potenza, Italy
Interests: transcriptional regulation; post-transcriptional regulation; miRNA; splicing mechanisms; liver
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The Special Issue, “Mitochondrial Metabolism in Health and Disease”, will focus on mitochondrial metabolism and function under physiological and pathological conditions. Mitochondria are hubs of bioenergetic metabolism generating ATP and biosynthetic precursors for macromolecules, oxidating fatty acids and amino acids and participating in redox homeostasis.

The main pathway is the Krebs cycle, which produces reducing equivalents to be sent to the respiratory chain for the ATP synthesis. At the same time, the intermediates of the Krebs cycle—beyond being needed for biosynthesis of macromolecules—together with mitochondrial ROS and mitochondrial proteins participate in the signaling networks mediating the cellular function in physiological and pathological conditions.

Metabolic-related mitochondrial signaling is also involved in the crosstalk between the mitochondria and the nucleus, whose knowledge allows a better understanding of human disorders. Remarkably, the deregulation of mitochondrial signaling plays a critical role in cancer, inflammation as well as countless diseases.

Additionally, mitochondrial dynamic processes and metabolism are strictly related to maintaining mitochondrial health, and mitochondrial structural remodeling also seems to be critical to the organelle’s function in light of the relationship between alterations of this process and pathophysiology of metabolic disease.

There is a large body of evidence linking unbalanced mitochondrial dynamics, including mitochondrial fusion/fission, mitochondrial biogenesis and mitophagy to aging-related cellular processes and several pathological conditions such as neurodegenerative diseases.

For this Special Issue, we are seeking contributions of original research or review articles ranging from mitochondrial bioenergetics to mitochondrial signaling, dynamics and nuclear-mitochondrial crosstalk to improve our understanding of the central role of mitochondria in cell function in health and disease. Submissions for this Special Issue may also relate to emerging mitochondrial target metabolites for diagnosis or treatment of mitochondrial diseases.

This Special Issue includes, but is not limited to, the following topics:

  1. Mitochondrial bioenergetics;
  2. Mitochondrial diseases;
  3. Mitochondrial signaling;
  4. Mitochondrial reprogramming metabolism;
  5. Anti-inflammatory signaling;
  6. Mitochondrial biogenesis/mitophagy;
  7. Mitochondrial structural remodeling.

Dr. Simona Todisco
Dr. Vittoria Infantino
Dr. Paolo Convertini
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. 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
  • bioenergetics
  • metabolism
  • mitochondrial dynamics
  • mitochondrial signaling
  • mitochondrial–nucleus crosstalk
  • mitochondrial biogenesis

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Published Papers (6 papers)

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Research

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15 pages, 3111 KiB  
Article
Mitochondrial Role in Intrinsic Apoptosis Induced by a New Synthesized Chalcone in Hepatocellular Carcinoma Cells
by Anna Santarsiero, Ilaria Pappalardo, Gabriella Margherita Rosa, Isabella Pisano, Stefano Superchi, Paolo Convertini, Simona Todisco, Patrizia Scafato and Vittoria Infantino
Biomedicines 2022, 10(12), 3120; https://doi.org/10.3390/biomedicines10123120 - 2 Dec 2022
Cited by 7 | Viewed by 1493
Abstract
Hepatocellular carcinoma (HCC) is the most common type of liver cancer and the fourth cause of cancer-related deaths worldwide. Presently, a few drugs are available for HCC treatment and prevention, including both natural and synthetic compounds. In this study, a new chalcone, ( [...] Read more.
Hepatocellular carcinoma (HCC) is the most common type of liver cancer and the fourth cause of cancer-related deaths worldwide. Presently, a few drugs are available for HCC treatment and prevention, including both natural and synthetic compounds. In this study, a new chalcone, (E)-1-(2,4,6-triethoxyphenyl)-3-(3,4,5-trimethoxyphenyl)prop-2-en-1-one (ETTC), was synthesized and its effects and mechanisms of action over human hepatoma cells were investigated. Cytotoxic activity was revealed in HCC cells, while no effects were observed in normal hepatocytes. In HCC cells, ETTC caused subG1 cell cycle arrest and apoptosis, characterized by nuclear fragmentation. The activation of caspases 3/7 and 9, the increase in pro-apoptotic BAX, and the decrease in anti-apoptotic BCL-2 suggest the activation of the intrinsic pathway of apoptosis. ETTC mitochondrial targeting is confirmed by the reduction in mitochondrial membrane potential and Complex I activity together with levels of superoxide anion increasing. Our outcomes prove the potential mitochondria-mediated antitumor effect of newly synthesized chalcone ETTC in HCC. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism in Health and Disease)
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19 pages, 2490 KiB  
Article
In Vivo and Ex Vivo Mitochondrial Function in COVID-19 Patients on the Intensive Care Unit
by Lucia W. J. M. Streng, Calvin J. de Wijs, Nicolaas J. H. Raat, Patricia A. C. Specht, Dimitri Sneiders, Mariëlle van der Kaaij, Henrik Endeman, Egbert G. Mik and Floor A. Harms
Biomedicines 2022, 10(7), 1746; https://doi.org/10.3390/biomedicines10071746 - 20 Jul 2022
Cited by 9 | Viewed by 2088
Abstract
Mitochondrial dysfunction has been linked to disease progression in COVID-19 patients. This observational pilot study aimed to assess mitochondrial function in COVID-19 patients at intensive care unit (ICU) admission (T1), seven days thereafter (T2), and in healthy controls and a general anesthesia group. [...] Read more.
Mitochondrial dysfunction has been linked to disease progression in COVID-19 patients. This observational pilot study aimed to assess mitochondrial function in COVID-19 patients at intensive care unit (ICU) admission (T1), seven days thereafter (T2), and in healthy controls and a general anesthesia group. Measurements consisted of in vivo mitochondrial oxygenation and oxygen consumption, in vitro assessment of mitochondrial respiration in platelet-rich plasma (PRP) and peripheral blood mononuclear cells (PBMCs), and the ex vivo quantity of circulating cell-free mitochondrial DNA (mtDNA). The median mitoVO2 of COVID-19 patients on T1 and T2 was similar and tended to be lower than the mitoVO2 in the healthy controls, whilst the mitoVO2 in the general anesthesia group was significantly lower than that of all other groups. Basal platelet (PLT) respiration did not differ substantially between the measurements. PBMC basal respiration was increased by approximately 80% in the T1 group when contrasted to T2 and the healthy controls. Cell-free mtDNA was eight times higher in the COVID-T1 samples when compared to the healthy controls samples. In the COVID-T2 samples, mtDNA was twofold lower when compared to the COVID-T1 samples. mtDNA levels were increased in COVID-19 patients but were not associated with decreased mitochondrial O2 consumption in vivo in the skin, and ex vivo in PLT or PBMC. This suggests the presence of increased metabolism and mitochondrial damage. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism in Health and Disease)
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23 pages, 4846 KiB  
Article
Traumatic and Diabetic Schwann Cell Demyelination Is Triggered by a Transient Mitochondrial Calcium Release through Voltage Dependent Anion Channel 1
by Nicolas Tricaud, Benoit Gautier, Jade Berthelot, Sergio Gonzalez and Gerben Van Hameren
Biomedicines 2022, 10(6), 1447; https://doi.org/10.3390/biomedicines10061447 - 19 Jun 2022
Cited by 4 | Viewed by 2677
Abstract
A large number of peripheral neuropathies, among which are traumatic and diabetic peripheral neuropathies, result from the degeneration of the myelin sheath, a process called demyelination. Demyelination does not result from Schwann cell death but from Schwann cell dedifferentiation, which includes reprograming and [...] Read more.
A large number of peripheral neuropathies, among which are traumatic and diabetic peripheral neuropathies, result from the degeneration of the myelin sheath, a process called demyelination. Demyelination does not result from Schwann cell death but from Schwann cell dedifferentiation, which includes reprograming and several catabolic and anabolic events. Starting around 4 h after nerve injury, activation of MAPK/cJun pathways is the earliest characterized step of this dedifferentiation program. Here we show, using real-time in vivo imaging, that Schwann cell mitochondrial pH, motility and calcium content are altered as soon as one hour after nerve injury. Mitochondrial calcium release occurred through the VDAC outer membrane channel and mPTP inner membrane channel. This calcium influx in the cytoplasm induced Schwann-cell demyelination via MAPK/c-Jun activation. Blocking calcium release through VDAC silencing or VDAC inhibitor TRO19622 prevented demyelination. We found that the kinetics of mitochondrial calcium release upon nerve injury were altered in the Schwann cells of diabetic mice suggesting a permanent leak of mitochondrial calcium in the cytoplasm. TRO19622 treatment alleviated peripheral nerve defects and motor deficit in diabetic mice. Together, these data indicate that mitochondrial calcium homeostasis is instrumental in the Schwann cell demyelination program and that blocking VDAC constitutes a molecular basis for developing anti-demyelinating drugs for diabetic peripheral neuropathy. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism in Health and Disease)
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Review

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19 pages, 1667 KiB  
Review
Targeting Mitochondrial DNA Transcription by POLRMT Inhibition or Depletion as a Potential Strategy for Cancer Treatment
by Sabrina C. D. Daglish, Emily M. J. Fennell and Lee M. Graves
Biomedicines 2023, 11(6), 1598; https://doi.org/10.3390/biomedicines11061598 - 31 May 2023
Cited by 3 | Viewed by 3858
Abstract
Transcription of the mitochondrial genome is essential for the maintenance of oxidative phosphorylation (OXPHOS) and other functions directly related to this unique genome. Considerable evidence suggests that mitochondrial transcription is dysregulated in cancer and cancer metastasis and contributes significantly to cancer cell metabolism. [...] Read more.
Transcription of the mitochondrial genome is essential for the maintenance of oxidative phosphorylation (OXPHOS) and other functions directly related to this unique genome. Considerable evidence suggests that mitochondrial transcription is dysregulated in cancer and cancer metastasis and contributes significantly to cancer cell metabolism. Recently, inhibitors of the mitochondrial DNA-dependent RNA polymerase (POLRMT) were identified as potentially attractive new anti-cancer compounds. These molecules (IMT1, IMT1B) inactivate cancer cell metabolism through reduced transcription of mitochondrially-encoded OXPHOS subunits such as ND1-5 (Complex I) and COI-IV (Complex IV). Studies from our lab have discovered small molecule regulators of the mitochondrial matrix caseinolytic protease (ClpP) as probable inhibitors of mitochondrial transcription. These compounds activate ClpP proteolysis and lead to the rapid depletion of POLRMT and other matrix proteins, resulting in inhibition of mitochondrial transcription and growth arrest. Herein we present a comparison of POLRMT inhibition and ClpP activation, both conceptually and experimentally, and evaluate the results of these treatments on mitochondrial transcription, inhibition of OXPHOS, and ultimately cancer cell growth. We discuss the potential for targeting mitochondrial transcription as a cancer cell vulnerability. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism in Health and Disease)
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14 pages, 1814 KiB  
Review
Targeting Mitochondrial Function with Chemoptogenetics
by Amy Romesberg and Bennett Van Houten
Biomedicines 2022, 10(10), 2459; https://doi.org/10.3390/biomedicines10102459 - 1 Oct 2022
Cited by 5 | Viewed by 1883
Abstract
Mitochondria are ATP-generating organelles in eukaryotic cells that produce reactive oxygen species (ROS) during oxidative phosphorylation (OXPHOS). Mitochondrial DNA (mtDNA) is packaged within nucleoids and, due to its close proximity to ROS production, endures oxidative base damage. This damage can be repaired by [...] Read more.
Mitochondria are ATP-generating organelles in eukaryotic cells that produce reactive oxygen species (ROS) during oxidative phosphorylation (OXPHOS). Mitochondrial DNA (mtDNA) is packaged within nucleoids and, due to its close proximity to ROS production, endures oxidative base damage. This damage can be repaired by base excision repair (BER) within the mitochondria, or it can be degraded via exonucleases or mitophagy. Persistent mtDNA damage may drive the production of dysfunctional OXPHOS components that generate increased ROS, or OXPHOS components may be directly damaged by ROS, which then can cause more mtDNA damage and create a vicious cycle of ROS production and mitochondrial dysfunction. If mtDNA damage is left unrepaired, mtDNA mutations including deletions can result. The accumulation of mtDNA mutations has been associated with conditions ranging from the aging process to cancer and neurodegenerative conditions, but the sequence of events leading to mtDNA mutations and deletions is yet unknown. Researchers have utilized many systems and agents for generating ROS in mitochondria to observe the downstream effects on mtDNA, ROS, and mitochondrial function; yet, there are various drawbacks to these methodologies that limit their precision. Here, we describe a novel chemoptogenetic approach to target oxidative damage to mitochondria and mtDNA with a high spatial and temporal resolution so that the downstream effects of ROS-induced damage can be measured with a high precision in order to better understand the mechanism of mitochondrial dysfunction in aging, cancer, and neurodegenerative diseases. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism in Health and Disease)
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13 pages, 1314 KiB  
Review
Updates on the Pivotal Roles of Mitochondria in Urothelial Carcinoma
by Chiang-Chi Huang, Hui-Ying Liu, Tsuen-Wei Hsu and Wen-Chin Lee
Biomedicines 2022, 10(10), 2453; https://doi.org/10.3390/biomedicines10102453 - 1 Oct 2022
Cited by 2 | Viewed by 1584
Abstract
Mitochondria are important organelles responsible for energy production, redox homeostasis, oncogenic signaling, cell death, and apoptosis. Deregulated mitochondrial metabolism and biogenesis are often observed during cancer development and progression. Reports have described the crucial roles of mitochondria in urothelial carcinoma (UC), which is [...] Read more.
Mitochondria are important organelles responsible for energy production, redox homeostasis, oncogenic signaling, cell death, and apoptosis. Deregulated mitochondrial metabolism and biogenesis are often observed during cancer development and progression. Reports have described the crucial roles of mitochondria in urothelial carcinoma (UC), which is a major global health challenge. This review focuses on research advances in the role of mitochondria in UC. Here, we discuss the pathogenic roles of mitochondria in UC and update the mitochondria-targeted therapies. We aim to offer a better understanding of the mitochondria-modulated pathogenesis of UC and hope that this review will allow the development of novel mitochondria-targeted therapies. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism in Health and Disease)
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