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Mitochondrial dynamics and the significance of its disturbances in the development of childhood diseases. Part I. Physiological and neurological aspects ; Митохондриальная динамика и значение ее нарушений в развитии детских болезней. Часть I. Физиологические и неврологические аспекты

Title: Mitochondrial dynamics and the significance of its disturbances in the development of childhood diseases. Part I. Physiological and neurological aspects ; Митохондриальная динамика и значение ее нарушений в развитии детских болезней. Часть I. Физиологические и неврологические аспекты
Authors: V. S. Sukhorukov; T. I. Baranich; A. V. Egorova; E. N. Fedorova; K. A. Skvortsova; D. A. Kharlamov; A. I. Krapivkin; В. С. Сухоруков; Т. И. Баранич; А. В. Егорова; Е. Н. Федорова; К. А. Скворцова; Д. А. Харламов; А. И. Крапивкин
Source: Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics); Том 69, № 1 (2024); 25-33 ; Российский вестник перинатологии и педиатрии; Том 69, № 1 (2024); 25-33 ; 2500-2228 ; 1027-4065
Publisher Information: Ltd. “The National Academy of Pediatric Science and Innovation”
Publication Year: 2024
Collection: Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) / Российский вестник перинатологии и педиатрии
Subject Terms: болезни нервной системы; mitochondria; mitochondrial dynamics; mitochondrial fission; mitochondrial fusion; histogenesis; tissue homeostasis; neurological diseases; митохондрии; митохондриальная динамика; деление митохондрий; слияние митохондрий; гистогенез; тканевой гомеостаз
Description: In recent years, the dynamics of mitochondrial transformations in cells have been of more concern to both representatives of basic science and researchers in the field of applied medicine. A growing number of observations demonstrate the important regulatory influence of mitochondrial dynamics on a variety of physiological and pathological processes in many, if not all, organ and tissue structures. The prospects for studying the features and regulators of these processes for understanding the pathogenesis of diseases, developing their new biomarkers, as well as treatment technologies seem increasingly significant. The purpose of this article is to review the facts obtained regarding mitochondrial dynamics, which, from the authors’ point of view, deserve the attention of pediatricians. The volume of relevant information turned out to be too extensive to fit into one article, which forced it to be divided into several successive publications. The first part provides information about the main processes included in the concept of “mitochondrial dynamics,” the importance of maintaining the balance of the latter for ontogenesis and tissue homeostasis, as well as data on its disturbances in diseases of the nervous system in children. ; Динамика митохондриальных преобразований в клетке вызывает в последние годы все больший интерес как представителей фундаментальной науки, так и исследователей в области прикладной медицины. Растет число наблюдений, доказывающих важное регуляторное влияние митохондриальной динамики на разнообразные физиологические и патологические процессы во многих, если не во всех, органных и тканевых структурах. Представляются все более важными перспективы изучения особенностей и регуляторов этих процессов для понимания патогенеза заболеваний, разработки их новых биомаркеров, а также технологий лечения. Цель настоящей статьи — обзор полученных в отношении митохондриальной динамики фактов, которые с точки зрения авторов заслуживают внимания педиатров. Объем соответствующей информации оказался слишком ...
Document Type: article in journal/newspaper
File Description: application/pdf
Language: Russian
Relation: https://www.ped-perinatology.ru/jour/article/view/1935/1455; Popov L.D. Mitochondrial biogenesis: An update. J Cell Mol Med 2020; 24(9): 4892–4899. DOI:10.1111/jcmm.15194; Sprenger H.G., Langer T. The Good and the Bad of Mitochondrial Breakups. Trends Cell Biol 2019; 29(11): 888–900. DOI:10.1016/j.tcb.2019.08.003; Kleele T., Rey T., Winter J., Zaganelli S., Mahecic D., Perreten Lambert H. et al. Distinct fission signatures predict mitochondrial degradation or biogenesis. Nature 2021; 593 (7859): 435–439. DOI:10.1038/s41586–021–03510–6; Chiu Y.H., Lin S.A., Kuo C.H., Li C.J. Molecular Machinery and Pathophysiology of Mitochondrial Dynamics. Front Cell Dev Biol 2021; 9: 743892. DOI:10.3389/fcell.2021.743892; Jones A., Thornton C. Mitochondrial dynamics in the neonatal brain — a potential target following injury? Biosci Rep 2022; 42(3): BSR20211696. DOI:10.1042/BSR20211696; Friedman J.R., Lackner L.L., West M., DiBenedetto J.R., Nunnari J., Voeltz G.K. ER tubules mark sites of mitochondrial division. Science 2011; 334(6054): 358–362. DOI:10.1126/science.1207385; Sukhorukov V.S., Voronkova A.S., Baranich T.I., Gofman A.A., Brydun A.V., Knyazeva L.A. et al. Molecular Mechanisms of Interactions between Mitochondria and the Endoplasmic Reticulum: A New Look at How Important Cell Functions are Supported. Mol Biol (Mosk) 2022; 56: 69–82. Russian. DOI:10.31857/S0026898422010098; Narendra D.P., Youle R.J. Targeting mitochondrial dysfunction: role for PINK1 and Parkin in mitochondrial quality control. Antioxid Redox Signal 2011; 14(10): 1929–1938. DOI:10.1089/ars.2010.3799; Chan D.C. Mitochondrial Dynamics and Its Involvement in Disease. Annu Rev Pathol 2020; 15: 235–259. DOI:10.1146/annurev-pathmechdis-012419–032711; Adebayo M., Singh S., Singh A.P., Dasgupta S. Mitochondrial fusion and fission: The fine-tune balance for cellular homeostasis. FASEB J 2021; 35(6): e21620. DOI:10.1096/fj.202100067R; Meeusen S., McCaffery J.M., Nunnari J. Mitochondrial fusion intermediates revealed in vitro. Science 2004; 305(5691): 1747–1752. DOI:10.1126/science.1100612; Malka F., Guillery O., Cifuentes-Diaz C., Guillou E., Belenguer P., Lombès A. et al. Separate fusion of outer and inner mitochondrial membranes. EMBO Rep 2005; 6(9): 853–859. DOI:10.1038/sj.embor.7400488; Ban T., Ishihara T., Kohno H., Saita S., Ichimura A., Maenaka K. et al. Molecular basis of selective mitochondrial fusion by heterotypic action between OPA1 and cardiolipin. Nat Cell Biol 2017; 19(7): 856–863. DOI:10.1038/ncb3560; Zhu T., Hu Q., Yuan Y., Yao H., Zhang J., Qi J. Mitochondrial dynamics in vascular remodeling and target-organ damage. Front Cardiovasc Med 2023; 10: 1067732. DOI:10.3389/fcvm.2023.1067732; Tilokani L., Nagashima S., Paupe V., Prudent J. Mitochondrial dynamics: overview of molecular mechanisms. Essays Biochem 2018; 62(3): 341–360. DOI:10.1042/EBC20170104; de Brito O.M., Scorrano L. Mitofusin 2 tethers endoplasmic reticulum to mitochondria. Nature 2008; 456(7222): 605–610. DOI:10.1038/nature07534. Erratum in: Nature 2014; 513 (7517): 266; Santel A., Frank S., Gaume B., Herrler M., Youle R.J., Fuller M.T. Mitofusin-1 protein is a generally expressed mediator of mitochondrial fusion in mammalian cells. J Cell Sci 2003; 116(Pt 13): 2763–2774. DOI:10.1242/jcs.00479; Mattie S., Riemer J., Wideman J.G., McBride H.M. A new mitofusin topology places the redox-regulated C terminus in the mitochondrial intermembrane space. J Cell Biol 2018; 217(2): 507–515. DOI:10.1083/jcb.201611194; Ishihara N., Fujita Y., Oka T., Mihara K. Regulation of mitochondrial morphology through proteolytic cleavage of OPA1. EMBO J 2006; 25(13): 2966–2977. DOI:10.1038/sj.emboj.7601184; Song Z., Chen H., Fiket M., Alexander C., Chan D.C. OPA1 processing controls mitochondrial fusion and is regulated by mRNA splicing, membrane potential, and Yme1L. J Cell Biol 2007; 178(5): 749–755. DOI:10.1083/jcb.200704110; Liu X., Weaver D., Shirihai O., Hajnóczky G. Mitochondrial ‘kiss-and-run’: interplay between mitochondrial motility and fusion-fission dynamics. EMBO J 2009; 28(20): 3074–3089. DOI:10.1038/emboj.2009.255; Yao C.H., Wang R., Wang Y., Kung C.P., Weber J.D., Patti G.J. Mitochondrial fusion supports increased oxidative phosphorylation during cell proliferation. Elife 2019; 8: e41351. DOI:10.7554/eLife.41351; Ng M.Y.W., Wai T., Simonsen A. Quality control of the mitochondrion. Dev Cell 2021; 56(7): 881–905. DOI:10.1016/j.devcel.2021.02.009; Wolf D.M., Segawa M., Kondadi A.K., Anand R., Bailey S.T., Reichert A.S. et al. Individual cristae within the same mitochondrion display different membrane potentials and are functionally independent. EMBO J 2019; 38(22): e101056. DOI:10.15252/embj.2018101056; Feng X., Zhang W., Yin W., Kang Y.J. The involvement of mitochondrial fission in maintenance of the stemness of bone marrow mesenchymal stem cells. Exp Biol Med (Maywood) 2019; 244(1): 64–72. DOI:10.1177/1535370218821063; Ren L., Chen X., Chen X., Li J., Cheng B., Xia J. Mitochondrial Dynamics: Fission and Fusion in Fate Determination of Mesenchymal Stem Cells. Front Cell Dev Biol 2020; 8: 580070. DOI:10.3389/fcell.2020.580070; Son M.J., Kwon Y., Son M.Y., Seol B., Choi H.S., Ryu S.W. et al. Mitofusins deficiency elicits mitochondrial metabolic reprogramming to pluripotency. Cell Death Differ 2015; 22(12): 1957–1969. DOI:10.1038/cdd.2015.43; Zhong X., Cui P., Cai Y., Wang L., He X., Long P. et al. Mitochondrial Dynamics Is Critical for the Full Pluripotency and Embryonic Developmental Potential of Pluripotent Stem Cells. Cell Metab 2019; 29(4): 979–992.e4. DOI:10.1016/j.cmet.2018.11.007; Fujiwara M., Tian L., Le P.T., DeMambro V.E., Becker K.A., Rosen C.J. et al. The mitophagy receptor Bcl-2-like protein 13 stimulates adipogenesis by regulating mitochondrial oxidative phosphorylation and apoptosis in mice. J Biol Chem 2019; 294(34): 12683–12694. DOI:10.1074/jbc.RA119.008630; Forni M.F., Peloggia J., Trudeau K., Shirihai O., Kowaltowski A.J. Murine Mesenchymal Stem Cell Commitment to Differentiation Is Regulated by Mitochondrial Dynamics. Stem Cells 2016; 34(3): 743–755. DOI:10.1002/stem.2248; Fang D., Yan S., Yu Q., Chen D., Yan S.S. Mfn2 is Required for Mitochondrial Development and Synapse Formation in Human Induced Pluripotent Stem Cells/hiPSC Derived Cortical Neurons. Sci Rep 2016; 6: 31462. DOI:10.1038/srep31462; Luchsinger L.L., de Almeida M.J., Corrigan D.J., Mumau M., Snoeck H.W. Mitofusin 2 maintains haematopoietic stem cells with extensive lymphoid potential. Nature 2016; 529(7587): 528–531. DOI:10.1038/nature16500; Yapa N.M.B., Lisnyak V., Reljic B., Ryan M.T. Mitochondrial dynamics in health and disease. FEBS Lett 2021; 595(8): 1184–1204. DOI:10.1002/1873–3468.14077; Green A., Hossain T., Eckmann D.M. Mitochondrial dynamics involves molecular and mechanical events in motility, fusion and fission. Front Cell Dev Biol 2022; 10: 1010232. DOI:10.3389/fcell.2022.1010232; Al Ojaimi M., Salah A., El-Hattab A.W. Mitochondrial Fission and Fusion: Molecular Mechanisms, Biological Functions, and Related Disorders. Membranes (Basel) 2022; 12(9): 893. DOI:10.3390/membranes12090893; Pareyson D., Saveri P., Pisciotta C. New developments in Charcot-Marie-Tooth neuropathy and related diseases. Curr Opin Neurol 2017; 30(5): 471–480. DOI:10.1097/WCO.0000000000000474; Horvath R., Medina J., Reilly M.M., Shy M.E., Zuchner S. Peripheral neuropathy in mitochondrial disease. Handb Clin Neurol 2023; 194: 99–116. DOI:10.1016/B978–0–12–821751–1.00014–2; Liu Y.T., Laurá M., Hersheson J., Horga A., Jaunmuktane Z., Brandner S. et al. Extended phenotypic spectrum of KIF5A mutations: From spastic paraplegia to axonal neuropathy. Neurology 2014; 83(7): 612–619. DOI:10.1212/WNL.0000000000000691; Shirokova O.M., Pchelin P.V., Mukhina I.V. MERCs. The Novel Assistant to Neurotransmission? Front Neurosci 2020; 14: 589319. DOI:10.3389/fnins.2020.589319; Zaman M., Shutt T.E. The Role of Impaired Mitochondrial Dynamics in MFN2-Mediated Pathology. Front Cell Dev Biol 2022; 10: 858286. DOI:10.3389/fcell.2022.858286; Gu Y., Guerra F., Hu M., Pope A., Sung K., Yang W. et al. Mitochondria dysfunction in Charcot Marie Tooth 2B Peripheral Sensory Neuropathy. Commun Biol 2022; 5(1): 717. DOI:10.1038/s42003–022–03632–1; Hagberg H., Mallard C., Rousset C.I., Thornton C. Mitochondria: hub of injury responses in the developing brain. Lancet Neurol 2014; 13(2): 217–232. DOI:10.1016/S1474–4422(13)70261–8; Cowell R.M., Blake K.R., Russell J.W. Localization of the transcriptional coactivator PGC-1alpha to GABAergic neurons during maturation of the rat brain. J Comp Neurol 2007; 502(1): 1–18. DOI:10.1002/cne.21211; Jia L., Wang J., Cao H., Zhang X., Rong W., Xu Z. Activation of PGC-1α and Mitochondrial Biogenesis Protects Against Prenatal Hypoxic-ischemic Brain Injury. Neuroscience 2020; 432: 63–72. DOI:10.1016/j.neuroscience.2020.02.035; Agarwal S., Yadav A., Chaturvedi R.K. Peroxisome proliferator-activated receptors (PPARs) as therapeutic target in neurodegenerative disorders. Biochem Biophys Res Commun 2017; 483(4): 1166–1177. DOI:10.1016/j.bbrc.2016.08.043; Arteaga O., Revuelta M., Urigüen L., Álvarez A., Montalvo H., Hilario E. Pretreatment with Resveratrol Prevents Neuronal Injury and Cognitive Deficits Induced by Perinatal Hypoxia-Ischemia in Rats. PLoS One 2015; 10(11): e0142424. DOI:10.1371/journal.pone.0142424; Baburamani A.A., Hurling C., Stolp H., Sobotka K., Gressens P., Hagberg H. et al. Mitochondrial Optic Atrophy (OPA) 1 Processing Is Altered in Response to Neonatal Hypoxic-Ischemic Brain Injury. Int J Mol Sci 2015; 16(9): 22509–22526. DOI:10.3390/ijms160922509; Vannucci R.C., Vannucci S.J. A model of perinatal hypoxic-ischemic brain damage. Ann N Y Acad Sci 1997; 835: 234–249. DOI:10.1111/j.1749–6632.1997.tb48634.x; Demarest T.G., Waite E.L., Kristian T., Puche A.C., Waddell J., McKenna M.C. et al. Sex-dependent mitophagy and neuronal death following rat neonatal hypoxia-ischemia. Neuroscience 2016; 335: 103–113. DOI:10.1016/j.neuroscience.2016.08.026; Cheng M., Lin N., Dong D., Ma J., Su J., Sun L. PGAM5: A crucial role in mitochondrial dynamics and programmed cell death. Eur J Cell Biol 2021; 100(1): 151144. DOI:10.1016/j.ejcb.2020.151144; Vongsfak J., Pratchayasakul W., Apaijai N., Vaniyapong T., Chattipakorn N., Chattipakorn S.C. The Alterations in Mitochondrial Dynamics Following Cerebral Ischemia/Reperfusion Injury. Antioxidants (Basel) 2021; 10(9): 1384. DOI:10.3390/antiox10091384; Huang J., Chen L., Yao Z.M., Sun X.R., Tong X.H., Dong S.Y. The role of mitochondrial dynamics in cerebral ischemia-reperfusion injury. Biomed Pharmacother 2023; 162: 114671. DOI:10.1016/j.biopha.2023.114671; Sharma J., Johnston M.V., Hossain M.A. Sex differences in mitochondrial biogenesis determine neuronal death and survival in response to oxygen glucose deprivation and reoxygenation. BMC Neurosci 2014; 15: 9. DOI:10.1186/1471–2202–15–9; Quebedeaux T.M., Song H., Giwa-Otusajo J., Thompson L.P. Chronic Hypoxia Inhibits Respiratory Complex IV Activity and Disrupts Mitochondrial Dynamics in the Fetal Guinea Pig Forebrain. Reprod Sci 2022; 29(1): 184–192. DOI:10.1007/s43032–021–00779-w; Mikhail A.I., Ng S.Y., Mattina S.R., Ljubicic V. AMPK is mitochondrial medicine for neuromuscular disorders. Trends Mol Med 2023; 29(7): 512–529. DOI:10.1016/j.molmed.2023.03.008; Zilio E., Piano V., Wirth B. Mitochondrial Dysfunction in Spinal Muscular Atrophy. Int J Mol Sci 2022; 23(18): 10878. DOI:10.3390/ijms231810878; Xu C.C., Denton K.R., Wang Z.B., Zhang X., Li X.J. Abnormal mitochondrial transport and morphology as early pathological changes in human models of spinal muscular atrophy. Dis Model Mech 2016; 9(1): 39–49. DOI:10.1242/dmm.021766; Thelen M.P., Wirth B., Kye M.J. Mitochondrial defects in the respiratory complex I contribute to impaired translational initiation via ROS and energy homeostasis in SMA motor neurons. Acta Neuropathol Commun 2020; 8(1): 223. DOI:10.1186/s40478–020–01101–6; Wang Y., Xu C., Ma L., Mou Y., Zhang B., Zhou S. et al. Drug screening with human SMN2 reporter identifies SMN protein stabilizers to correct SMA pathology. Life Sci Alliance 2019; 2(2): e201800268. DOI:10.26508/lsa.201800268; Ripolone M., Ronchi D., Violano R., Vallejo D., Fagiolari G., Barca E. et al. Impaired Muscle Mitochondrial Biogenesis and Myogenesis in Spinal Muscular Atrophy. JAMA Neurol 2015; 72(6): 666–675. DOI:10.1001/jamaneurol.2015.0178; Strauss M., Hofhaus G., Schröder R.R., Kühlbrandt W. Dimer ribbons of ATP synthase shape the inner mitochondrial membrane. EMBO J 2008; 27(7): 1154–60. DOI:10.1038/emboj.2008.35; Isashiki Y., Kawabata E., Ohba N., Higuchi I., Nakagawa M., Osame M. Mitochondrial abnormalities in extraocular muscles in myotonic dystrophy. Neuro-Opthalmology 1989; 9: 115–122. DOI:10.3109/01658108909007466; Mikhail A.I., Manta A., Ng S.Y., Osborne A.K., Mattina S.R., Mackie M.R. et al. A single dose of exercise stimulates skeletal muscle mitochondrial plasticity in myotonic dystrophy type 1. Acta Physiol (Oxf) 2023; 237(4): e13943. DOI:10.1111/apha.13943; Moore T.M., Lin A.J., Strumwasser A.R., Cory K., Whitney K., Ho T. et al. Mitochondrial Dysfunction Is an Early Consequence of Partial or Complete Dystrophin Loss in mdx Mice. Front Physiol 2020; 11: 690. DOI:10.3389/fphys.2020.00690; Hardee J.P., Caldow M.K., Chan A.S.M., Plenderleith S.K., Trieu J., Koopman R. et al. Dystrophin deficiency disrupts muscle clock expression and mitochondrial quality control in mdx mice. Am J Physiol Cell Physiol 2021; 321(2): C288–C296. DOI:10.1152/ajpcell.00188.2021; Харламов Д.А., Крапивкин А.И., Сухоруков В.С., Куфтина Л.А., Грознова О.С. Неврологические нарушения при митохондриальной энцефаломиопатии — лактатацидозе с инсультоподобными эпизодами (синдроме MELAS). Российский вестник перинатологии и педиатрии 2012; 4(2): 36–42.; Burgin H.J., Lopez Sanchez M.I.G., Smith C.M., Trounce I.A., McKenzie M. Pioglitazone and Deoxyribonucleoside Combination Treatment Increases Mitochondrial Respiratory Capacity in m.3243A>G MELAS Cybrid Cells. Int J Mol Sci 2020; 21(6): 2139. DOI:10.3390/ijms21062139
DOI: 10.21508/1027-4065-2024-69-1-25-33
Availability: https://www.ped-perinatology.ru/jour/article/view/1935; https://doi.org/10.21508/1027-4065-2024-69-1-25-33
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Database: BASE