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Axonal mitophagy in retinal ganglion cells
Neurons, exhibiting unique polarized structures, rely primarily on the mitochondrial production of ATP to maintain their hypermetabolic energy requirements. To maintain a normal energy supply, mitochondria are transported to the distal end of the axon. When mitochondria within the axon are criticall...
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| Published in: | Cell communication and signaling 2024-07, Vol.22 (1), p.382-12, Article 382 |
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| container_title | Cell communication and signaling |
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| creator | Liang, Yang Li, Yulin Jiao, Qing Wei, Muyang Wang, Yan Cui, Aoteng Li, Zhihui Li, Guangyu |
| description | Neurons, exhibiting unique polarized structures, rely primarily on the mitochondrial production of ATP to maintain their hypermetabolic energy requirements. To maintain a normal energy supply, mitochondria are transported to the distal end of the axon. When mitochondria within the axon are critically damaged beyond their compensatory capacity, they are cleared via autophagosomal phagocytosis, and the degradation products are recycled to replenish energy. When the mitochondria are dysfunctional or their transport processes are blocked, axons become susceptible to degeneration triggered by energy depletion, resulting in neurodegenerative diseases. As the final checkpoint for mitochondrial quality control, axonal mitophagy is vital for neuronal growth, development, injury, and regeneration. Furthermore, abnormal axonal mitophagy is crucial in the pathogenesis of optic nerve-related diseases such as glaucoma. We review recent studies on axonal mitophagy and summarize the progress of research on axonal mitophagy in optic nerve-related diseases to provide insights into diseases associated with axonal damage in optic ganglion cells. |
| doi_str_mv | 10.1186/s12964-024-01761-0 |
| format | article |
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To maintain a normal energy supply, mitochondria are transported to the distal end of the axon. When mitochondria within the axon are critically damaged beyond their compensatory capacity, they are cleared via autophagosomal phagocytosis, and the degradation products are recycled to replenish energy. When the mitochondria are dysfunctional or their transport processes are blocked, axons become susceptible to degeneration triggered by energy depletion, resulting in neurodegenerative diseases. As the final checkpoint for mitochondrial quality control, axonal mitophagy is vital for neuronal growth, development, injury, and regeneration. Furthermore, abnormal axonal mitophagy is crucial in the pathogenesis of optic nerve-related diseases such as glaucoma. We review recent studies on axonal mitophagy and summarize the progress of research on axonal mitophagy in optic nerve-related diseases to provide insights into diseases associated with axonal damage in optic ganglion cells.</description><identifier>ISSN: 1478-811X</identifier><identifier>EISSN: 1478-811X</identifier><identifier>DOI: 10.1186/s12964-024-01761-0</identifier><identifier>PMID: 39075570</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Animals ; Autophagy ; Autophagy (Cytology) ; Axon ; Axonal transport ; Axonogenesis ; Axons - metabolism ; Axons - pathology ; Biosynthesis ; Care and treatment ; Degradation products ; Diagnosis ; Disease ; Disease susceptibility ; Energy ; Energy requirements ; Ganglion ; Glaucoma ; Health aspects ; Humans ; Kinases ; Mitochondria ; Mitochondria - metabolism ; Mitochondria - pathology ; Mitochondrial DNA ; Mitophagy ; Neurodegeneration ; Neurodegenerative diseases ; Optic nerve ; Oxidative phosphorylation ; Parkinson's disease ; Phagocytosis ; Phosphorylation ; Physiology ; Proteins ; Quality control ; Regeneration ; Retinal ganglion cells ; Retinal Ganglion Cells - metabolism ; Retinal Ganglion Cells - pathology ; Review ; RNA polymerase</subject><ispartof>Cell communication and signaling, 2024-07, Vol.22 (1), p.382-12, Article 382</ispartof><rights>2024. The Author(s).</rights><rights>COPYRIGHT 2024 BioMed Central Ltd.</rights><rights>2024. This work is licensed under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2024 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c479t-dc1f59f29c7419cb3bdb6b4d28d48c57c045e346d230ce8d6b3830ace291f8c13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11285280/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/3091293912?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39075570$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liang, Yang</creatorcontrib><creatorcontrib>Li, Yulin</creatorcontrib><creatorcontrib>Jiao, Qing</creatorcontrib><creatorcontrib>Wei, Muyang</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Cui, Aoteng</creatorcontrib><creatorcontrib>Li, Zhihui</creatorcontrib><creatorcontrib>Li, Guangyu</creatorcontrib><title>Axonal mitophagy in retinal ganglion cells</title><title>Cell communication and signaling</title><addtitle>Cell Commun Signal</addtitle><description>Neurons, exhibiting unique polarized structures, rely primarily on the mitochondrial production of ATP to maintain their hypermetabolic energy requirements. To maintain a normal energy supply, mitochondria are transported to the distal end of the axon. When mitochondria within the axon are critically damaged beyond their compensatory capacity, they are cleared via autophagosomal phagocytosis, and the degradation products are recycled to replenish energy. When the mitochondria are dysfunctional or their transport processes are blocked, axons become susceptible to degeneration triggered by energy depletion, resulting in neurodegenerative diseases. As the final checkpoint for mitochondrial quality control, axonal mitophagy is vital for neuronal growth, development, injury, and regeneration. Furthermore, abnormal axonal mitophagy is crucial in the pathogenesis of optic nerve-related diseases such as glaucoma. We review recent studies on axonal mitophagy and summarize the progress of research on axonal mitophagy in optic nerve-related diseases to provide insights into diseases associated with axonal damage in optic ganglion cells.</description><subject>Analysis</subject><subject>Animals</subject><subject>Autophagy</subject><subject>Autophagy (Cytology)</subject><subject>Axon</subject><subject>Axonal transport</subject><subject>Axonogenesis</subject><subject>Axons - metabolism</subject><subject>Axons - pathology</subject><subject>Biosynthesis</subject><subject>Care and treatment</subject><subject>Degradation products</subject><subject>Diagnosis</subject><subject>Disease</subject><subject>Disease susceptibility</subject><subject>Energy</subject><subject>Energy requirements</subject><subject>Ganglion</subject><subject>Glaucoma</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>Mitochondrial DNA</subject><subject>Mitophagy</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Optic nerve</subject><subject>Oxidative phosphorylation</subject><subject>Parkinson's disease</subject><subject>Phagocytosis</subject><subject>Phosphorylation</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Quality control</subject><subject>Regeneration</subject><subject>Retinal ganglion cells</subject><subject>Retinal Ganglion Cells - metabolism</subject><subject>Retinal Ganglion Cells - pathology</subject><subject>Review</subject><subject>RNA polymerase</subject><issn>1478-811X</issn><issn>1478-811X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkt1r1TAYxoMobk7_AS_kgDc66MybpGlyJYeh24HBwA_wLqRJ2uXQNsekle2_N93Z5ioj5IO3v_cJefog9BbwCYDgnxIQyVmBSZ5QcSjwM3QIrBKFAPj1_NH5AL1KaYszWbLqJTqgEldlWeFDdLy-DoPuVr0fw-5KtzcrP6yiG_1cbPXQdj4MK-O6Lr1GLxrdJffmbj9CP79--XF6Xlxcnm1O1xeFYZUcC2ugKWVDpKkYSFPT2ta8ZpYIy4QpK4NZ6SjjllBsnLC8poJibRyR0AgD9Aht9ro26K3aRd_reKOC9uq2EGKrdBy96ZyqHaGmcWA1towaLqwkteUAlmpJGpe1Pu-1dlPdO2vcMEbdLUSXXwZ_pdrwRwEQURKBs8KHO4UYfk8ujar3afZDDy5MSVEsOOYku5zR9_-h2zDFbORMyfyzaF7-Ua3OL_BDE_LFZhZV63wfYC6FzNTJE1Qe1vXehME1PtcXDR8XDZkZ3fXY6ikltfn-bcmSPWtiSCm65sEQwGqOltpHS-XAqNtoqdmId4-tfGi5zxL9C7LnxtY</recordid><startdate>20240729</startdate><enddate>20240729</enddate><creator>Liang, Yang</creator><creator>Li, Yulin</creator><creator>Jiao, Qing</creator><creator>Wei, Muyang</creator><creator>Wang, Yan</creator><creator>Cui, Aoteng</creator><creator>Li, Zhihui</creator><creator>Li, Guangyu</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</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>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20240729</creationdate><title>Axonal mitophagy in retinal ganglion cells</title><author>Liang, Yang ; Li, Yulin ; Jiao, Qing ; Wei, Muyang ; Wang, Yan ; Cui, Aoteng ; Li, Zhihui ; Li, Guangyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-dc1f59f29c7419cb3bdb6b4d28d48c57c045e346d230ce8d6b3830ace291f8c13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Autophagy</topic><topic>Autophagy (Cytology)</topic><topic>Axon</topic><topic>Axonal transport</topic><topic>Axonogenesis</topic><topic>Axons - metabolism</topic><topic>Axons - pathology</topic><topic>Biosynthesis</topic><topic>Care and treatment</topic><topic>Degradation products</topic><topic>Diagnosis</topic><topic>Disease</topic><topic>Disease susceptibility</topic><topic>Energy</topic><topic>Energy requirements</topic><topic>Ganglion</topic><topic>Glaucoma</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - pathology</topic><topic>Mitochondrial DNA</topic><topic>Mitophagy</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative diseases</topic><topic>Optic nerve</topic><topic>Oxidative phosphorylation</topic><topic>Parkinson's disease</topic><topic>Phagocytosis</topic><topic>Phosphorylation</topic><topic>Physiology</topic><topic>Proteins</topic><topic>Quality control</topic><topic>Regeneration</topic><topic>Retinal ganglion cells</topic><topic>Retinal Ganglion Cells - metabolism</topic><topic>Retinal Ganglion Cells - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cell communication and signaling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liang, Yang</au><au>Li, Yulin</au><au>Jiao, Qing</au><au>Wei, Muyang</au><au>Wang, Yan</au><au>Cui, Aoteng</au><au>Li, Zhihui</au><au>Li, Guangyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Axonal mitophagy in retinal ganglion cells</atitle><jtitle>Cell communication and signaling</jtitle><addtitle>Cell Commun Signal</addtitle><date>2024-07-29</date><risdate>2024</risdate><volume>22</volume><issue>1</issue><spage>382</spage><epage>12</epage><pages>382-12</pages><artnum>382</artnum><issn>1478-811X</issn><eissn>1478-811X</eissn><abstract>Neurons, exhibiting unique polarized structures, rely primarily on the mitochondrial production of ATP to maintain their hypermetabolic energy requirements. To maintain a normal energy supply, mitochondria are transported to the distal end of the axon. When mitochondria within the axon are critically damaged beyond their compensatory capacity, they are cleared via autophagosomal phagocytosis, and the degradation products are recycled to replenish energy. When the mitochondria are dysfunctional or their transport processes are blocked, axons become susceptible to degeneration triggered by energy depletion, resulting in neurodegenerative diseases. As the final checkpoint for mitochondrial quality control, axonal mitophagy is vital for neuronal growth, development, injury, and regeneration. Furthermore, abnormal axonal mitophagy is crucial in the pathogenesis of optic nerve-related diseases such as glaucoma. We review recent studies on axonal mitophagy and summarize the progress of research on axonal mitophagy in optic nerve-related diseases to provide insights into diseases associated with axonal damage in optic ganglion cells.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>39075570</pmid><doi>10.1186/s12964-024-01761-0</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Animals Autophagy Autophagy (Cytology) Axon Axonal transport Axonogenesis Axons - metabolism Axons - pathology Biosynthesis Care and treatment Degradation products Diagnosis Disease Disease susceptibility Energy Energy requirements Ganglion Glaucoma Health aspects Humans Kinases Mitochondria Mitochondria - metabolism Mitochondria - pathology Mitochondrial DNA Mitophagy Neurodegeneration Neurodegenerative diseases Optic nerve Oxidative phosphorylation Parkinson's disease Phagocytosis Phosphorylation Physiology Proteins Quality control Regeneration Retinal ganglion cells Retinal Ganglion Cells - metabolism Retinal Ganglion Cells - pathology Review RNA polymerase |
| title | Axonal mitophagy in retinal ganglion cells |
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