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Special Issue "Mitochondrial Function in Health and Disease 3.0"

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

Deadline for manuscript submissions: 10 December 2023 | Viewed by 5998

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Prof. Dr. Galina D. Mironova

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Guest Editor

Laboratory of Mitochondrial Transport, Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Institutskaya 3, Pushchino, 142290 Moscow, Russia
Interests: ion permeability; ion channels; mitochondria; mitoK(ATP) channels; palmitate/calcium-induced permeability transition pore; phospholipases; mitochondrial transplantation; oxidative stress; hypoxia; ischemia/reperfusion; neurodegenerative diseases
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Dr. Natalia Belosludtseva

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Guest Editor

Laboratory of Mitochondrial Transport, Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Institutskaya 3, Pushchino, 142290 Moscow, Russia
Interests: membrane permeability; artificial membranes; ion channels; mitochondria; mitochondrial permeability transition pore; palmitate/calcium-induced permeability transition pore; calcium uniporter; mitochondrial dynamics; biogenesis; mitophagy; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are important subcellular organelles that play pivotal roles in ATP production, the regulation of calcium ion homeostasis, oxidative metabolism, the biosynthesis of amino acids, nucleic acids, lipids, hemes, and purines, steroidogenesis, thermogenesis, cell division, immune response, and programmed cell death. A growing body of evidence indicates that mitochondria are deeply involved in the generation and scavenging of reactive oxygen species (ROS) in the cell, ensuring the maintenance of cellular redox homeostasis. Recent data suggest that adaptive and maladaptive responses to mitochondrial redox stress may involve ion transport systems, including the mitochondrial permeability transition pores, calcium uniporter complex, and potassium channels. An enhanced steady-state level of mitochondrial ROS may have deleterious consequences due to oxidative damage to biomolecules and, hence, mitochondrial ultrastructure.

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning the role of mitochondria in cellular physiology and oxidative-stress-related diseases. The research can include both in vitro and in vivo studies relating to potential therapeutic approaches to restore mitochondrial function in cell and animal models of disease.

We look forward to your contribution.

Prof. Dr. Galina D. Mironova
Dr. Natalia Belosludtseva
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

mitochondrial function
ultrastructural alterations
oxidative phosphorylation
mitochondrial ion channels
mitochondrial permeability transition pores
mitochondrial defensive antioxidant systems
oxidative stress
mitophagy
apoptosis
mitochondria-targeted therapeutic strategies
antioxidant therapy

Published Papers (5 papers)

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Research

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Open AccessArticle

Codium fragile Suppresses PM_2.5-Induced Cognitive Dysfunction by Regulating Gut–Brain Axis via TLR-4/MyD88 Pathway

and

Int. J. Mol. Sci. 2023, 24(16), 12898; https://doi.org/10.3390/ijms241612898 - 17 Aug 2023

Viewed by 633

Abstract

This study was conducted to evaluate the cognitive dysfunction improvement effect of aqueous extract of Codium fragile (AECF) by regulating the imbalance of the gut–brain axis in chronic particulate matter (PM)_2.5-exposed mice. The physiological compounds of AECF were identified as hexadecanamide, oleamide, octadecanamide, stearidonic acid, and linolenic acid by the ultra-performance liquid chromatography-quadrupole time of flight mass spectrometry (UPLC Q-TOF MS^E) analysis. To evaluate the effect of PM_2.5 on the antioxidant system, superoxide dismutase (SOD) contents, reduced glutathione (GSH) contents, and malondialdehyde (MDA) contents were measured in colon and brain tissues. AECF significantly ameliorated the imbalance of the antioxidant systems. Also, AECF improved intestinal myeloperoxidase (MPO) activity, the abundance of the gut microbiome, short-chain fatty acids (SCFAs) contents, and tight junction protein expression against PM_2.5-induced damage. In addition, AECF prevented PM_2.5-induced inflammatory and apoptotic expression via the toll-like receptor-4 (TLR-4)/myeloid differentiation primary response 88 (MyD88) pathway in colon and brain tissues. Additionally, AECF enhanced the mitochondrial function, including the mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) contents in brain tissues. Furthermore, AECF regulated the cholinergic system, such as acetylcholine (ACh) contents, acetylcholinesterase (AChE) activity, and protein expression levels of AChE and choline acetyltransferase (ChAT) in brain tissues. To evaluate the effect of cognitive dysfunction caused by PM_2.5-induced intestinal dysfunction, behavior tests such as Y-maze, passive avoidance, and Morris water maze tests were performed. From the results of the behavior tests, AECF ameliorated spatial learning and memory, short-term memory, and long-term learning and memory function. This study confirmed that AECF reduced PM_2.5-induced cognitive dysfunction by regulating gut microbiome and inflammation, apoptosis, and mitochondrial function by enhancing the gut–brain axis. Based on these results, this study suggests that AECF, which contains fatty acid amides, might be a potential material for ameliorating PM_2.5-induced cognitive dysfunction via gut–brain axis improvement. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 3.0)

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Open AccessArticle

Regulation of Mitochondrial Permeability Transition Pore Opening by Monovalent Cations in Liver Mitochondria

Ekaterina S. Kharechkina

Anna B. Nikiforova

and

Alexey G. Kruglov

Int. J. Mol. Sci. 2023, 24(11), 9237; https://doi.org/10.3390/ijms24119237 - 25 May 2023

Viewed by 668

Abstract

The opening of the permeability transition pore (PTP) in mitochondria is a key event in the initiation of cell death in various pathologic states, including ischemia/reperfusion. The activation of K⁺ transport into mitochondria protects cells from ischemia/reperfusion. However, the role of K⁺ transport in PTP regulation is unclear. Here, we studied the role of K⁺ and other monovalent cations in the regulation of the PTP opening in an in vitro model. The registration of the PTP opening, membrane potential, Ca²⁺-retention capacity, matrix pH, and K⁺ transport was performed using standard spectral and electrode techniques. We found that the presence of all cations tested in the medium (K⁺, Na⁺, choline⁺, and Li⁺) strongly stimulated the PTP opening compared with sucrose. Several possible reasons for this were examined: the effect of ionic strength, the influx of cations through selective and non-selective channels and exchangers, the suppression of Ca²⁺/H⁺ exchange, and the influx of anions. The data obtained indicate that the mechanism of PTP stimulation by cations includes the suppression of K⁺/H⁺ exchange and acidification of the matrix, which facilitates the influx of phosphate. Thus, the K⁺/H⁺ exchanger and the phosphate carrier together with selective K⁺ channels compose a PTP regulatory triad, which might operate in vivo. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 3.0)

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Open AccessArticle

Ultrastructural Evidence of Mitochondrial Dysfunction in Osteomyelitis Patients

and

Christoph Brochhausen

Int. J. Mol. Sci. 2023, 24(6), 5709; https://doi.org/10.3390/ijms24065709 - 16 Mar 2023

Viewed by 1261

Abstract

Osteomyelitis is a difficult-to-treat disease with high chronification rates. First studies suggest increases in mitochondrial fission and mitochondrial dysfunction as possible contributors to the accumulation of intracellular reactive oxygen species and thereby to the cell death of infected bone cells. The aim of the present study is to analyze the ultrastructural impact of bacterial infection on osteocytic and osteoblastic mitochondria. Human infected bone tissue samples were visualized via light microscopy and transmission electron microscopy. Osteoblasts, osteocytes and their mitochondria were analyzed histomorphometrically and compared with the control group of noninfectious human bone tissue samples. The results depicted swollen hydropic mitochondria including depleted cristae and a decrease in matrix density in the infected samples. Furthermore, perinuclear clustering of mitochondria could also be observed regularly. Additionally, increases in relative mitochondrial area and number were found as a correlate for increased mitochondrial fission. In conclusion, mitochondrial morphology is altered during osteomyelitis in a comparable way to mitochondria from hypoxic tissues. This gives new perspectives on the treatment strategies since the manipulation of mitochondrial dynamics may improve bone cell survival as a potential new target for the therapy of osteomyelitis. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 3.0)

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Open AccessArticle

A Comparative Study on the Effects of the Lysine Reagent Pyridoxal 5-Phosphate and Some Thiol Reagents in Opening the Tl⁺-Induced Mitochondrial Permeability Transition Pore

Sergey M. Korotkov

and

Artemy V. Novozhilov

Int. J. Mol. Sci. 2023, 24(3), 2460; https://doi.org/10.3390/ijms24032460 - 27 Jan 2023

Viewed by 753

Abstract

Lysine residues are essential in regulating enzymatic activity and the spatial structure maintenance of mitochondrial proteins and functional complexes. The most important parts of the mitochondrial permeability transition pore are F1F0 ATPase, the adenine nucleotide translocase (ANT), and the inorganic phosphate cotransporter. The ANT conformation play a significant role in the Tl⁺-induced MPTP opening in the inner membrane of calcium-loaded rat liver mitochondria. The present study tests the effects of a lysine reagent, pyridoxal 5-phosphate (PLP), and thiol reagents (phenylarsine oxide, tert-butylhydroperoxide, eosin-5-maleimide, and mersalyl) to induce the MPTP opening that was accompanied by increased swelling, membrane potential decline, and decreased respiration in 3 and 3U_DNP (2,4-dinitrophenol uncoupled) states. This pore opening was more noticeable in increasing the concentration of PLP and thiol reagents. However, more significant concentrations of PLP were required to induce the above effects comparable to those of these thiol reagents. This study suggests that the Tl⁺-induced MPTP opening can be associated not only with the state of functionally active cysteines of the pore parts, but may be due to a change in the state of the corresponding lysines forming the pore structure. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 3.0)

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The Tricky Connection between Extracellular Vesicles and Mitochondria in Inflammatory-Related Diseases

Tommaso Di Mambro

Giulia Pellielo

Esther Densu Agyapong

and

Int. J. Mol. Sci. 2023, 24(9), 8181; https://doi.org/10.3390/ijms24098181 - 03 May 2023

Cited by 2 | Viewed by 2062

Abstract

Mitochondria are organelles present in almost all eukaryotic cells, where they represent the main site of energy production. Mitochondria are involved in several important cell processes, such as calcium homeostasis, OXPHOS, autophagy, and apoptosis. Moreover, they play a pivotal role also in inflammation through the inter-organelle and inter-cellular communications, mediated by the release of mitochondrial damage-associated molecular patterns (mtDAMPs). It is currently well-documented that in addition to traditional endocrine and paracrine communication, the cells converse via extracellular vesicles (EVs). These small membrane-bound particles are released from cells in the extracellular milieu under physio-pathological conditions. Importantly, EVs have gained much attention for their crucial role in inter-cellular communication, translating inflammatory signals into recipient cells. EVs cargo includes plasma membrane and endosomal proteins, but EVs also contain material from other cellular compartments, including mitochondria. Studies have shown that EVs may transport mitochondrial portions, proteins, and/or mtDAMPs to modulate the metabolic and inflammatory responses of recipient cells. Overall, the relationship between EVs and mitochondria in inflammation is an active area of research, although further studies are needed to fully understand the mechanisms involved and how they may be targeted for therapeutic purposes. Here, we have reported and discussed the latest studies focused on this fascinating and recent area of research, discussing of tricky connection between mitochondria and EVs in inflammatory-related diseases. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 3.0)

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