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Mitochondrial Transfer in Various Conditions
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Mitochondrial Transfer in Various Conditions

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (15 March 2021) | Viewed by 22645

Special Issue Editor

Prof. Dr. Satoshi Gojo

E-Mail Website
Guest Editor
Department of Regenerative Medicine, Kyoto Prefectural University of Medicine, 465 Kajii cho, Kamigyo ku, Kyoto 602-8655, Japan
Interests: mitochondrial biology; lysosomal biology; organelle; RNA decay; gene therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Although horizontal gene transfer has played an essential role to evolve bacteria and archaea, its existence in eukaryotes has been underestimated for a long time. Since the discovery of intercellular transfer of mitochondria under in vitro culture condition, in vivo mitochondrial transfer has been reported upon a pathological stress in various organs, including the brain and the lung. Because mitochondria are not only powerhouses but also hubs of intracellular innate immunity, the consequence of mitochondrial transfer could depend on context. Already, the prevention of mitochondrial diseases by taking advantage of artificial mitochondrial transfer and replacement to in vitro fertilization has been proposed, raising serious ethical issues, and isolated mitochondrial transplantation to the failed heart, expecting to be engulfed into cardiomyocytes, has been applied in a clinical arena. For ex vivo gene therapy for mitochondrial DNA and more sophisticated mitochondria transplantation, in vitro methods to transfer exogeneous mitochondria more effectively have been intensively investigated. Although some clinical applications are very progressive, the relationship between the nuclear genome and mitochondrial DNA still remains mysterious, and a strategy to prevent the stimulation their innate immunity and apoptosis has to be established. It could help to more safely and effectively treat diseases and gather interdisciplinarily research related to mitochondrial transfer. 

  • Topics:
    • Mitochondrial biology;
    • Mitochondrial dynamics;
    • Innate immunity;
    • Autophagy;
    • Mitochondrial diseases;
    • Neurodegenerative diseases;
    • Infertility;
    • Cancer biology;
    • Autoimmune disorders.

Prof. Satoshi Gojo
Guest Editor

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Keywords

  • Mitochondrial transfer
  • Mitochondrial replacement
  • Heteroplasmy
  • Respirometry
  • OXPHOS and glycolysis
  • Tunneling nanotube
  • Exome
  • Mitochondrial DNA
  • Reactive oxygen species
  • NACHT, LRR, and PYD domains containing protein 3 (NALP3)
  • Mitochondrial antiviral-signaling protein (MAVS)
  • Nuclear and mitochondrial interactions
  • Reversion

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Published Papers (4 papers)

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Research

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14 pages, 2317 KiB  
Article
Long-Chain and Medium-Chain Fatty Acids in Energy Metabolism of Murine Kidney Mitochondria
by Alexander V. Panov, Vladimir I. Mayorov, Anna E. Dikalova and Sergey I. Dikalov
Int. J. Mol. Sci. 2023, 24(1), 379; https://doi.org/10.3390/ijms24010379 - 26 Dec 2022
Cited by 16 | Viewed by 3378
Abstract
Scientists have long established that fatty acids are the primary substrates for kidney mitochondria. However, to date we still do not know how long-chain and middle-chain fatty acids are oxidized at the mitochondrial level. Our previous research has shown that mitochondria from the [...] Read more.
Scientists have long established that fatty acids are the primary substrates for kidney mitochondria. However, to date we still do not know how long-chain and middle-chain fatty acids are oxidized at the mitochondrial level. Our previous research has shown that mitochondria from the heart, brain, and kidney oxidize palmitoylcarnitine at a high rate only in the presence of succinate, glutamate, or pyruvate. In this paper, we report properties of the isolated kidney mitochondria and how malate and succinate affect the oxidation of C16 and C8 acylcarnitines. The isolated kidney mitochondria contain very few endogenous substrates and require malate to oxidize pyruvate, glutamate, and C16 or C8 acylcarnitines. We discovered that with 10 µM of C16 or C8 acylcarnitines, low concentrations of malate (0.2 mM) or succinate (0.5 mM) enhance the States 4 and 3 respiratory rates several times. The highest respiration rates were observed with C16 or C8 acylcarnitines and 5 mM succinate mixtures. Results show that kidney mitochondria, unlike the heart and brain mitochondria, lack the intrinsic inhibition of succinate dehydrogenase. Additionally, results show that the oxidation of fatty acid by the small respirasome’s supercomplex generates a high level of CoQH2, and this makes SDH in the presence of succinate reverse the flow of electrons from CoQH2 to reduce fumarate to succinate. Finally, we report evidence that succinate dehydrogenase is a key mitochondrial enzyme that allows fast oxidation of fatty acids and turns the TCA cycle function from the catabolic to the anabolic and anaplerotic metabolic pathways. Full article
(This article belongs to the Special Issue Mitochondrial Transfer in Various Conditions)
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Review

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17 pages, 1190 KiB  
Review
Challenges in Promoting Mitochondrial Transplantation Therapy
by Yuma Yamada, Momo Ito, Manae Arai, Mitsue Hibino, Takao Tsujioka and Hideyoshi Harashima
Int. J. Mol. Sci. 2020, 21(17), 6365; https://doi.org/10.3390/ijms21176365 - 2 Sep 2020
Cited by 74 | Viewed by 6901
Abstract
Mitochondrial transplantation therapy is an innovative strategy for the treatment of mitochondrial dysfunction. The approach has been reported to be useful in the treatment of cardiac ischemic reperfusion injuries in human clinical trials and has also been shown to be useful in animal [...] Read more.
Mitochondrial transplantation therapy is an innovative strategy for the treatment of mitochondrial dysfunction. The approach has been reported to be useful in the treatment of cardiac ischemic reperfusion injuries in human clinical trials and has also been shown to be useful in animal studies as a method for treating mitochondrial dysfunction in various tissues, including the heart, liver, lungs, and brain. On the other hand, there is no methodology for using preserved mitochondria. Research into the pharmaceutical formulation of mitochondria to promote mitochondrial transplantation therapy as the next step in treating many patients is urgently needed. In this review, we overview previous studies on the therapeutic effects of mitochondrial transplantation. We also discuss studies related to immune responses that occur during mitochondrial transplantation and methods for preserving mitochondria, which are key to their stability as medicines. Finally, we describe research related to mitochondrial targeting drug delivery systems (DDS) and discuss future perspectives of mitochondrial transplantation. Full article
(This article belongs to the Special Issue Mitochondrial Transfer in Various Conditions)
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13 pages, 1017 KiB  
Review
Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes
by Mitsutoshi Yamada, Kazuhiro Akashi, Reina Ooka, Kenji Miyado and Hidenori Akutsu
Int. J. Mol. Sci. 2020, 21(16), 5880; https://doi.org/10.3390/ijms21165880 - 16 Aug 2020
Cited by 11 | Viewed by 4557
Abstract
Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders [...] Read more.
Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders with no cure, in which mutated mtDNA is passed from mothers to offspring via maternal egg cytoplasm. Mitochondrial replacement (MR) is a genome transfer technology in which mtDNA carrying disease-related mutations is replaced by presumably disease-free mtDNA. This therapy aims at preventing the transmission of known disease-causing mitochondria to the next generation. Here, a proof of concept for the specific removal or editing of mtDNA disease-related mutations by genome editing is introduced. Although the amount of mtDNA carryover introduced into human oocytes during nuclear transfer is low, the safety of mtDNA heteroplasmy remains a concern. This is particularly true regarding donor-recipient mtDNA mismatch (mtDNA–mtDNA), mtDNA-nuclear DNA (nDNA) mismatch caused by mixing recipient nDNA with donor mtDNA, and mtDNA replicative segregation. These conditions can lead to mtDNA genetic drift and reversion to the original genotype. In this review, we address the current state of knowledge regarding nuclear transplantation for preventing the inheritance of mitochondrial diseases. Full article
(This article belongs to the Special Issue Mitochondrial Transfer in Various Conditions)
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17 pages, 1630 KiB  
Review
From Cell Entry to Engraftment of Exogenous Mitochondria
by Daisuke Kami and Satoshi Gojo
Int. J. Mol. Sci. 2020, 21(14), 4995; https://doi.org/10.3390/ijms21144995 - 15 Jul 2020
Cited by 11 | Viewed by 6953
Abstract
Mitochondrial transfer has been recognized to play a role in a variety of processes, ranging from fertilization to cancer and neurodegenerative diseases as well as mammalian horizontal gene transfer. It is achieved through either exogeneous or intercellular mitochondrial transfer. From the viewpoint of [...] Read more.
Mitochondrial transfer has been recognized to play a role in a variety of processes, ranging from fertilization to cancer and neurodegenerative diseases as well as mammalian horizontal gene transfer. It is achieved through either exogeneous or intercellular mitochondrial transfer. From the viewpoint of evolution, exogeneous mitochondrial transfer is quite akin to the initial process of symbiosis between α-protobacterium and archaea, although the progeny have developed more sophisticated machinery to engulf environmental materials, including nutrients, bacteria, and viruses. A molecular-based knowledge of endocytosis, including macropinocytosis and endosomal escape involving bacteria and viruses, could provide mechanistic insights into exogeneous mitochondrial transfer. We focus on exogeneous mitochondrial transfer in this review to facilitate the clinical development of the use of isolated mitochondria to treat various pathological conditions. Several kinds of novel procedures to enhance exogeneous mitochondrial transfer have been developed and are summarized in this review. Full article
(This article belongs to the Special Issue Mitochondrial Transfer in Various Conditions)
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