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Impaired Mitophagy in Neurons and Glial Cells during Aging and Age-Related Disorders
Aging is associated with a decline in cognitive function, which can partly be explained by the accumulation of damage to the brain cells over time. Neurons and glia undergo morphological and ultrastructure changes during aging. Over the past several years, it has become evident that at the cellular...
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| Published in: | International journal of molecular sciences 2021-09, Vol.22 (19), p.10251 |
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| container_issue | 19 |
| container_start_page | 10251 |
| container_title | International journal of molecular sciences |
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| creator | Sukhorukov, Vladimir Voronkov, Dmitry Baranich, Tatiana Mudzhiri, Natalia Magnaeva, Alina Illarioshkin, Sergey |
| description | Aging is associated with a decline in cognitive function, which can partly be explained by the accumulation of damage to the brain cells over time. Neurons and glia undergo morphological and ultrastructure changes during aging. Over the past several years, it has become evident that at the cellular level, various hallmarks of an aging brain are closely related to mitophagy. The importance of mitochondria quality and quantity control through mitophagy is highlighted by the contribution that defects in mitochondria-autophagy crosstalk make to aging and age-related diseases. In this review, we analyze some of the more recent findings regarding the study of brain aging and neurodegeneration in the context of mitophagy. We discuss the data on the dynamics of selective autophagy in neurons and glial cells during aging and in the course of neurodegeneration, focusing on three mechanisms of mitophagy: non-receptor-mediated mitophagy, receptor-mediated mitophagy, and transcellular mitophagy. We review the role of mitophagy in neuronal/glial homeostasis and in the molecular pathogenesis of neurodegenerative disorders, such as Parkinson's disease, Alzheimer's disease, and other disorders. Common mechanisms of aging and neurodegeneration that are related to different mitophagy pathways provide a number of promising targets for potential therapeutic agents. |
| doi_str_mv | 10.3390/ijms221910251 |
| format | article |
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Neurons and glia undergo morphological and ultrastructure changes during aging. Over the past several years, it has become evident that at the cellular level, various hallmarks of an aging brain are closely related to mitophagy. The importance of mitochondria quality and quantity control through mitophagy is highlighted by the contribution that defects in mitochondria-autophagy crosstalk make to aging and age-related diseases. In this review, we analyze some of the more recent findings regarding the study of brain aging and neurodegeneration in the context of mitophagy. We discuss the data on the dynamics of selective autophagy in neurons and glial cells during aging and in the course of neurodegeneration, focusing on three mechanisms of mitophagy: non-receptor-mediated mitophagy, receptor-mediated mitophagy, and transcellular mitophagy. 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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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We review the role of mitophagy in neuronal/glial homeostasis and in the molecular pathogenesis of neurodegenerative disorders, such as Parkinson's disease, Alzheimer's disease, and other disorders. Common mechanisms of aging and neurodegeneration that are related to different mitophagy pathways provide a number of promising targets for potential therapeutic agents.</description><subject>Age</subject><subject>Aging</subject><subject>Aging - pathology</subject><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Autophagy</subject><subject>Autophagy - physiology</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Chemical compounds</subject><subject>Crosstalk</subject><subject>Dopamine</subject><subject>Glial cells</subject><subject>Homeostasis</subject><subject>Homeostasis - physiology</subject><subject>Humans</subject><subject>Mitochondria</subject><subject>Mitochondria - pathology</subject><subject>Mitochondrial DNA</subject><subject>mitophagy</subject><subject>Mitophagy - physiology</subject><subject>Mutation</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative Diseases - pathology</subject><subject>Neuroglia - pathology</subject><subject>Neuronal-glial interactions</subject><subject>Neurons</subject><subject>Neurons - pathology</subject><subject>Oxidative stress</subject><subject>Parkinson's disease</subject><subject>Phagocytosis</subject><subject>Pharmacology</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Review</subject><subject>Ultrastructure</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkc1rFDEchoNYbK0evcqAl17G5vvjIiyr1oWqIPUcMvmYZpmZrMmM0P--2W4tXS9JyPvwkPxeAN4h-JEQBS_jdiwYI4UgZugFOEMU4xZCLl4-O5-C16VsIcQEM_UKnBLKiWRSnYGbzbgzMXvXfI9z2t2a_q6JU_PDLzlNpTGTa66GaIZm7YehNG7JceqbVb9f9-Gq9-0vP5i5Gj7HkrLzubwBJ8EMxb993M_B769fbtbf2uufV5v16rq1VKK5pcg5IinpguCEdtQK6K1QIhAhZAicGqGc75ASvGMKImaNtDV2nigWXCDnYHPwumS2epfjaPKdTibqh4uUe23yHO3gtYSUiMCEgYRT3hkDOSdKUoVQgLhT1fXp4Not3eid9dOczXAkPU6meKv79FdLBmVVVcHFoyCnP4svsx5jsXVqZvJpKRoziSTEUO3RD_-h27TkqY7qgYIUU4Er1R4om1Mp2YenxyCo993ro-4r__75D57of2WTexl1qQo</recordid><startdate>20210923</startdate><enddate>20210923</enddate><creator>Sukhorukov, Vladimir</creator><creator>Voronkov, Dmitry</creator><creator>Baranich, Tatiana</creator><creator>Mudzhiri, Natalia</creator><creator>Magnaeva, Alina</creator><creator>Illarioshkin, Sergey</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-5223-9767</orcidid><orcidid>https://orcid.org/0000-0002-2704-6282</orcidid><orcidid>https://orcid.org/0000-0002-0552-6939</orcidid><orcidid>https://orcid.org/0000-0001-5222-5322</orcidid></search><sort><creationdate>20210923</creationdate><title>Impaired Mitophagy in Neurons and Glial Cells during Aging and Age-Related Disorders</title><author>Sukhorukov, Vladimir ; 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| subjects | Age Aging Aging - pathology Alzheimer's disease Animals Autophagy Autophagy - physiology Brain damage Brain injury Chemical compounds Crosstalk Dopamine Glial cells Homeostasis Homeostasis - physiology Humans Mitochondria Mitochondria - pathology Mitochondrial DNA mitophagy Mitophagy - physiology Mutation Neurodegeneration Neurodegenerative Diseases - pathology Neuroglia - pathology Neuronal-glial interactions Neurons Neurons - pathology Oxidative stress Parkinson's disease Phagocytosis Pharmacology Phosphorylation Proteins Review Ultrastructure |
| title | Impaired Mitophagy in Neurons and Glial Cells during Aging and Age-Related Disorders |
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