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Mitochondrial Function in Health and Disease 2022

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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: closed (30 April 2023) | Viewed by 26255

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Prof. Dr. Galina D. Mironova

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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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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

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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 (11 papers)

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Research

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19 pages, 3567 KiB

Open AccessArticle

A Comparative Analysis of Neuroprotective Properties of Taxifolin and Its Water-Soluble Form in Ischemia of Cerebral Cortical Cells of the Mouse

by Elena G. Varlamova, Nina I. Uspalenko, Natalia V. Khmil, Maria I. Shigaeva, Mikhail R. Stepanov, Mikhail A. Ananyan, Maria A. Timchenko, Maxim V. Molchanov, Galina D. Mironova and Egor A. Turovsky

Int. J. Mol. Sci. 2023, 24(14), 11436; https://doi.org/10.3390/ijms241411436 - 14 Jul 2023

Cited by 5 | Viewed by 1227

Abstract

Cerebral ischemia, and, as a result, insult, attacks up to 15 million people yearly in the world. In this connection, the development of effective preventive programs and methods of therapy has become one of the most urgent problems in modern angiology and pharmacology. The cytoprotective action of taxifolin (TAX) in ischemia is well known, but its limitations are also known due to its poor solubility and low capacity to pass through the hematoencephalic barrier. Molecular mechanisms underlying the protective effect of TAX in complex systems such as the brain remain poorly understood. It is known that the main cell types of the brain are neurons, astrocytes, and microglia, which regulate the activity of each other through neuroglial interactions. In this work, a comparative study of cytoprotective mechanisms of the effect of TAX and its new water-soluble form aqua taxifolin (aqTAX) was performed on cultured brain cells under ischemia-like conditions (oxygen–glucose deprivation (OGD)) followed by the reoxygenation of the culture medium. The concentration dependences of the protective effects of both taxifolin forms were determined using fluorescence microscopy, PCR analysis, and vitality tests. It was found that TAX began to effectively inhibit necrosis and the late stages of apoptosis in the concentration range of 30–100 µg/mL, with aqTAX in the range of 10–30 µg/mL. At the level of gene expression, aqTAX affected a larger number of genes than TAX; enhanced the basic and OGD/R-induced expression of genes encoding ROS-scavenging proteins with a higher efficiency, as well as anti-inflammatory and antiapoptotic proteins; and lowered the level of excitatory glutamate receptors. As a result, aqTAX significantly inhibited the OGD-induced increase in the Ca²⁺ levels in the cytosol ([Ca²⁺]_i) in neurons and astrocytes under ischemic conditions. After a 40 min preincubation of cells with aqTAX under hypoxic conditions, these Ca²⁺ signals were completely inhibited, resulting in an almost complete suppression of necrotic death of cerebral cortical cells, which was not observed with the use of classical TAX. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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15 pages, 18859 KiB

Open AccessArticle

The Effect of Dietary Phospholipids on the Ultrastructure and Function of Intestinal Epithelial Cells

by Snezhanna Saydakova, Ksenia Morozova, Olga Snytnikova, Maryana Morozova, Lidiya Boldyreva, Elena Kiseleva, Yuri Tsentalovich and Elena Kozhevnikova

Int. J. Mol. Sci. 2023, 24(2), 1788; https://doi.org/10.3390/ijms24021788 - 16 Jan 2023

Cited by 1 | Viewed by 2167

Abstract

Dietary composition substantially determines human health and affects complex diseases, including obesity, inflammation and cancer. Thus, food supplements have been widely used to accommodate dietary composition to the needs of individuals. Among the promising supplements are dietary phospholipids (PLs) that are commonly found as natural food ingredients and as emulsifier additives. The aim of the present study was to evaluate the effect of major PLs found as food supplements on the morphology of intestinal epithelial cells upon short-term and long-term high-dose feeding in mice. In the present report, the effect of short-term and long-term high dietary PL content was studied in terms of intestinal health and leaky gut syndrome in male mice. We used transmission electron microscopy to evaluate endothelial morphology at the ultrastructural level. We found mitochondrial damage and lipid droplet accumulation in the intracristal space, which rendered mitochondria more sensitive to respiratory uncoupling as shown by a mitochondrial respiration assessment in the intestinal crypts. However, this mitochondrial damage was insufficient to induce intestinal permeability. We propose that high-dose PL treatment impairs mitochondrial morphology and acts through extensive membrane utilization via the mitochondria. The data suggest that PL supplementation should be used with precaution in individuals with mitochondrial disorders. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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16 pages, 3701 KiB

Open AccessArticle

Anti-Aging Effects of Anthocyanin Extracts of Sambucus canadensis Caused by Targeting Mitochondrial-Induced Oxidative Stress

by Xiaoqing Hu, Yimeng Yang, Shi Tang, Qiuyan Chen, Meiyu Zhang, Jiaoyan Ma, Jianchun Qin and Huimei Yu

Int. J. Mol. Sci. 2023, 24(2), 1528; https://doi.org/10.3390/ijms24021528 - 12 Jan 2023

Cited by 8 | Viewed by 2625

Abstract

Anthocyanin is a natural antioxidant agent extracted from the fruits of Sambucus canadensis, which has been considered to have potential anti-aging effects. Cell senescence is the primary cause of aging and related diseases. Recently, research on the development of compounds for eliminating senescent cells or damaged organs have shown prospects. The compounds which promote the clearing of senescent cells are called “senolytics”. Though anthocyanin is considered to have potential anti-aging effects owing to its anti-inflammatory and antioxidant activities, the mechanism of the elimination of senescent cells remains unclear. In this study, we prepared anthocyanins extracted from the fruits of Sambucus canadensis and evaluated their anti-aging effects in vivo and in vitro. We found that anthocyanin could significantly reduce cell senescence and aging of the lens by inhibiting the activity of the PI3K/AKT/mTOR signaling pathway, consequently promoting the apoptosis of senescent cells, increasing the autophagic and mitophagic flux, and enhancing the renewal of mitochondria and the cell to maintain cellular homeostasis, leading to attenuating aging. Therefore, our study provided a basis for anthocyanin to be used as new “senolytics” in anti-aging. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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15 pages, 12105 KiB

Open AccessArticle

MitoQ Protects Ovarian Organoids against Oxidative Stress during Oogenesis and Folliculogenesis In Vitro

by Jiapeng Wang, Hua Du, Lixin Ma, Mingqian Feng, Liping Li, Xiaorong Zhao and Yanfeng Dai

Int. J. Mol. Sci. 2023, 24(2), 924; https://doi.org/10.3390/ijms24020924 - 04 Jan 2023

Cited by 4 | Viewed by 2013

Abstract

Ovarian organoids, based on mouse female germline stem cells (FGSCs), have great value in basic research and are a vast prospect in pre-clinical drug screening due to their properties, but the competency of these in vitro-generated oocytes was generally low, especially, in vitro maturation (IVM) rate. Recently, it has been demonstrated that the 3D microenvironment triggers mitochondrial dysfunction during follicle growth in vitro. Therefore, therapies that protect mitochondria and enhance their function in oocytes warrant investigation. Here, we reported that exposure to 100 nM MitoQ promoted follicle growth and maturation in vitro, accompanied by scavenging ROS, reduced oxidative injury, and restored mitochondrial membrane potential in oocytes. Mechanistically, using mice granulosa cells (GCs) as a cellular model, it was shown that MitoQ protects GCs against H₂O₂-induced apoptosis by inhibiting the oxidative stress pathway. Together, these results reveal that MitoQ reduces oxidative stress in ovarian follicles via its antioxidative action, thereby protecting oocytes and granulosa cells and providing an efficient way to improve the quality of in vitro-generated oocytes. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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20 pages, 3020 KiB

Open AccessArticle

Altered Mitochondrial Morphology and Bioenergetics in a New Yeast Model Expressing Aβ42

by Khoren K. Epremyan, Anton G. Rogov, Tatyana N. Goleva, Svetlana V. Lavrushkina, Roman A. Zinovkin and Renata A. Zvyagilskaya

Int. J. Mol. Sci. 2023, 24(2), 900; https://doi.org/10.3390/ijms24020900 - 04 Jan 2023

Cited by 5 | Viewed by 1870

Abstract

Alzheimer’s disease (AD) is an incurable, age-related neurological disorder, the most common form of dementia. Considering that AD is a multifactorial complex disease, simplified experimental models are required for its analysis. For this purpose, genetically modified Yarrowia lipolytica yeast strains expressing Aβ42 (the main biomarker of AD), eGFP-Aβ42, Aβ40, and eGFP-Aβ40 were constructed and examined. In contrast to the cells expressing eGFP and eGFP-Aβ40, retaining “normal” mitochondrial reticulum, eGFP-Aβ42 cells possessed a disturbed mitochondrial reticulum with fragmented mitochondria; this was partially restored by preincubation with a mitochondria-targeted antioxidant SkQThy. Aβ42 expression also elevated ROS production and cell death; low concentrations of SkQThy mitigated these effects. Aβ42 expression caused mitochondrial dysfunction as inferred from a loose coupling of respiration and phosphorylation, the decreased level of ATP production, and the enhanced rate of hydrogen peroxide formation. Therefore, we have obtained the same results described for other AD models. Based on an analysis of these and earlier data, we suggest that the mitochondrial fragmentation might be a biomarker of the earliest preclinical stage of AD with an effective therapy based on mitochondria- targeted antioxidants. The simple yeast model constructed can be a useful platform for the rapid screening of such compounds. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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15 pages, 2100 KiB

Open AccessArticle

Metformin Alleviates Epirubicin-Induced Endothelial Impairment by Restoring Mitochondrial Homeostasis

by Qi Sun, Huiling Jia, Shuo Cheng, Yujuan Wang and Jun Wang

Int. J. Mol. Sci. 2023, 24(1), 343; https://doi.org/10.3390/ijms24010343 - 25 Dec 2022

Cited by 1 | Viewed by 1813

Abstract

Vascular endothelial injury is important in anthracycline-induced cardiotoxicity. Anthracyclines seriously damage the mitochondrial function and mitochondrial homeostasis. In this study, we investigated the damage of epirubicin to vascular endothelial cells and the protective role of metformin from the perspective of mitochondrial homeostasis. We found that epirubicin treatment resulted in DNA double-strand breaks (DSB), elevated reactive oxygen species (ROS) production, and excessive Angiotensin II release in HUVEC cells. Pretreatment with metformin significantly mitigated the injuries caused by epirubicin. In addition, inhibited expression of Mitochondrial transcription factor A (TFAM) and increased mitochondria fragmentation were observed in epirubicin-treated cells, which were partially resumed by metformin pretreatment. In epirubicin-treated cells, knockdown of TFAM counteracted the attenuated DSB formation due to metformin pretreatment, and inhibition of mitochondrial fragmentation with Mdivi-1 decreased DSB formation but increased TFAM expression. Furthermore, epirubicin treatment promoted mitochondrial fragmentation by stimulating the expression of Dynamin-1-like protein (DRP1) and inhibiting the expression of Optic atrophy-1(OPA1) and Mitofusin 1(MFN1), which could be partially prevented by metformin. Finally, we found metformin could increase TFAM expression and decrease DRP1 expression in epirubicin-treated HUVEC cells by upregulating the expression of calcineurin/Transcription factor EB (TFEB). Taken together, this study provided evidence that metformin treatment was an effective way to mitigate epirubicin-induced endothelial impairment by maintaining mitochondrial homeostasis. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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15 pages, 1405 KiB

Open AccessArticle

Insulin Diminishes Superoxide Increase in Cytosol and Mitochondria of Cultured Cortical Neurons Treated with Toxic Glutamate

by Vsevolod Pinelis, Irina Krasilnikova, Zanda Bakaeva, Alexander Surin, Dmitrii Boyarkin, Andrei Fisenko, Olga Krasilnikova and Igor Pomytkin

Int. J. Mol. Sci. 2022, 23(20), 12593; https://doi.org/10.3390/ijms232012593 - 20 Oct 2022

Cited by 6 | Viewed by 1755

Abstract

Glutamate excitotoxicity is involved in the pathogenesis of many disorders, including stroke, traumatic brain injury, and Alzheimer’s disease, for which central insulin resistance is a comorbid condition. Neurotoxicity of glutamate (Glu) is primarily associated with hyperactivation of the ionotropic N-methyl-D-aspartate receptors (NMDARs), causing a sustained increase in intracellular free calcium concentration ([Ca²⁺]_i) and synchronous mitochondrial depolarization and an increase in intracellular superoxide anion radical (O₂^–•) production. Recently, we found that insulin protects neurons against excitotoxicity by decreasing the delayed calcium deregulation (DCD). However, the role of insulin in O₂^–• production in excitotoxicity still needs to be clarified. The present study aims to investigate insulin’s effects on glutamate-evoked O₂^–• generation and DCD using the fluorescent indicators dihydroethidium, MitoSOX Red, and Fura-FF in cortical neurons. We found a linear correlation between [Ca²⁺]_i and [O₂^–•] in primary cultures of the rat neuron exposed to Glu, with insulin significantly reducing the production of intracellular and mitochondrial O₂^–• in the primary cultures of the rat neuron. MK 801, an inhibitor of NMDAR-gated Ca²⁺ influx, completely abrogated the glutamate effects in both the presence and absence of insulin. In experiments in sister cultures, insulin diminished neuronal death and O₂ consumption rate (OCR). Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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15 pages, 2691 KiB

Open AccessArticle

Effect of Chronic Treatment with Uridine on Cardiac Mitochondrial Dysfunction in the C57BL/6 Mouse Model of High-Fat Diet–Streptozotocin-Induced Diabetes

by Natalia V. Belosludtseva, Vlada S. Starinets, Irina B. Mikheeva, Maxim N. Belosludtsev, Mikhail V. Dubinin, Galina D. Mironova and Konstantin N. Belosludtsev

Int. J. Mol. Sci. 2022, 23(18), 10633; https://doi.org/10.3390/ijms231810633 - 13 Sep 2022

Cited by 8 | Viewed by 2643

Abstract

Long-term hyperglycemia in diabetes mellitus is associated with complex damage to cardiomyocytes and the development of mitochondrial dysfunction in the myocardium. Uridine, a pyrimidine nucleoside, plays an important role in cellular metabolism and is used to improve cardiac function. Herein, the antidiabetic potential of uridine (30 mg/kg/day for 21 days, i.p.) and its effect on mitochondrial homeostasis in the heart tissue were examined in a high-fat diet–streptozotocin-induced model of diabetes in C57BL/6 mice. We found that chronic administration of uridine to diabetic mice normalized plasma glucose and triglyceride levels and the heart weight/body weight ratio and increased the rate of glucose utilization during the intraperitoneal glucose tolerance test. Analysis of TEM revealed that uridine prevented diabetes-induced ultrastructural abnormalities in mitochondria and sarcomeres in ventricular cardiomyocytes. In diabetic heart tissue, the mRNA level of Ppargc1a decreased and Drp1 and Parkin gene expression increased, suggesting the disturbances of mitochondrial biogenesis, fission, and mitophagy, respectively. Uridine treatment of diabetic mice restored the mRNA level of Ppargc1a and enhanced Pink1 gene expression, which may indicate an increase in the intensity of mitochondrial biogenesis and mitophagy, and as a consequence, mitochondrial turnover. Uridine also reduced oxidative phosphorylation dysfunction and suppressed lipid peroxidation, but it had no significant effect on the impaired calcium retention capacity and potassium transport in the heart mitochondria of diabetic mice. Altogether, these findings suggest that, along with its hypoglycemic effect, uridine has a protective action against diabetes-mediated functional and structural damage to cardiac mitochondria and disruption of mitochondrial quality-control systems in the diabetic heart. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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16 pages, 3928 KiB

Open AccessArticle

Metformin Attenuates UVA-Induced Skin Photoaging by Suppressing Mitophagy and the PI3K/AKT/mTOR Pathway

by Qiuyan Chen, Haiying Zhang, Yimeng Yang, Shuming Zhang, Jing Wang, Dawei Zhang and Huimei Yu

Int. J. Mol. Sci. 2022, 23(13), 6960; https://doi.org/10.3390/ijms23136960 - 23 Jun 2022

Cited by 26 | Viewed by 4183

Abstract

Ultraviolet (UV) radiation is a major cause of photoaging that can induce DNA damage, oxidative stress, and cellular aging. Metformin (MF) can repair DNA damage, scavenge reactive oxygen species (ROS), and protect cells. However, the mechanism by which MF inhibits cell senescence in chronic skin damage induced by UVA is unclear. In this study, human foreskin fibroblasts (HFFs) treated with UVA were used as an in vitro model and UVA-induced skin photoaging in Kunming mice was used as an in vivo model to investigate the potential skin protective mechanism of MF. The results revealed that MF treatment attenuated UVA-induced cell viability, skin aging, and activation of the PI3K/AKT/mTOR signaling pathway. Furthermore, MF treatment alleviated the mitochondrial oxidative stress and decreased mitophagy. Knockdown of Parkin by siRNA increased the clearance of MF in senescent cells. The treatment of Kunming mice with MF at a dose of 10 mg/kg/day significantly reduced UVA-induced skin roughness, epidermal thinning, collagen degradation, and skin aging. In conclusion, our experimental results suggest that MF exerts anti-photoaging effects by inhibiting mitophagy and the PI3K/AKT/mTOR signaling pathway. Therefore, our study improves the current understanding of the protective mechanism of MF against photoaging. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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12 pages, 1887 KiB

Open AccessArticle

Does Trophectoderm Mitochondrial DNA Content Affect Embryo Developmental and Implantation Potential?

by Krzysztof Lukaszuk and Amira Podolak

Int. J. Mol. Sci. 2022, 23(11), 5976; https://doi.org/10.3390/ijms23115976 - 26 May 2022

Cited by 2 | Viewed by 1805

Abstract

A retrospective case control study was undertaken at the molecular biology department of a private center for reproductive medicine in order to determine whether any correlation exists between the mitochondrial DNA (mtDNA) content of trophectoderm and embryo developmental potential. A total of 275 couples underwent IVF treatment, producing a total of 716 embryos. The trophectoderm was biopsied from each embryo at the blastocyst stage (day 5 or day 6 post-fertilization) subjected to low-pass next-generation sequencing (NGS), for the purpose of detecting aneuploidy. For each sample, the number of mtDNA reads obtained after analysis using NGS was divided by the number of reads attributable to the nuclear genome. The mtDNA copy number was found to be higher in aneuploid embryos than in those that were euploid (mean mtDNA ratio ± SD: 1.13 ± 1.37 versus 1.45 ± 1.78, p = 0.02) and in day 5 biopsies compared to day 6 biopsies (1.41 ± 1.66 vs. 1.19 ± 1.27, p = 0.001), whereas no statistically significant differences in mtDNA content were seen in relation to embryo morphology (1.58 ± 2.44 vs. 2.19 ± 2.89, p = 0.12), genetic sex (1.27 ± 1.29 vs. 1.27 ± 1.18, p = 0.99), maternal age (1.31 ± 1.41 vs. 1.33 ± 1.29, p = 0.43), or its ability to implant (1.14 ± 0.88 vs. 1.21 ± 1.16, p = 0.39). mtDNA has small potential to serve as an additional, independent biomarker for embryo selection. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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Review

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19 pages, 3441 KiB

Open AccessReview

Advances in Human Mitochondria-Based Therapies

by Gang Zhong, Jagadeesh K. Venkatesan, Henning Madry and Magali Cucchiarini

Int. J. Mol. Sci. 2023, 24(1), 608; https://doi.org/10.3390/ijms24010608 - 29 Dec 2022

Cited by 4 | Viewed by 2549

Abstract

Mitochondria are the key biological generators of eukaryotic cells, controlling the energy supply while providing many important biosynthetic intermediates. Mitochondria act as a dynamic, functionally and structurally interconnected network hub closely integrated with other cellular compartments via biomembrane systems, transmitting biological information by shuttling between cells and tissues. Defects and dysregulation of mitochondrial functions are critically involved in pathological mechanisms contributing to aging, cancer, inflammation, neurodegenerative diseases, and other severe human diseases. Mediating and rejuvenating the mitochondria may therefore be of significant benefit to prevent, reverse, and even treat such pathological conditions in patients. The goal of this review is to present the most advanced strategies using mitochondria to manage such disorders and to further explore innovative approaches in the field of human mitochondria-based therapies. Full article

(This article belongs to the Special Issue Mitochondrial Function in Health and Disease 2022)

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