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Article: Restoration of optic neuropathy

TitleRestoration of optic neuropathy
Authors
Issue Date2017
PublisherDove Medical Press Ltd.(DovePress). The Journal's web site is located at http://www.dovepress.com/journal-of-neurorestoratology-journal
Citation
Journal of Neurorestoratology, 2017, v. 2017 n. 5, p. 59-72 How to Cite?
AbstractOptic neuropathy refers to disorders involving the optic nerve (ON). Any damage to ON or ON-deriving neurons, the retinal ganglion cells (RGCs), may lead to the breakdown of the optical signal transmission from the eye to the brain, thus resulting in a partial or complete vision loss. The causes of optic neuropathy include trauma, ischemia, inflammation, compression, infiltration, and mitochondrial damages. ON injuries include primary and secondary injuries. During these injury phases, various factors orchestrate injured axons to die back and become unable to regenerate, and these factors could be divided into two categories: extrinsic and intrinsic. Extrinsic inhibitory factors refer to the environmental conditions that influence the regeneration of injured axons. The presence of myelin inhibitors and glial scar, lack of neurotrophic factors, and inflammation mediated by injury are regarded as these extrinsic factors. Extrinsic factors need to trigger the intracellular signals to exert inhibitory effect. Proper regulation of these intracellular signals has been shown to be beneficial to ON regeneration. Intrinsic factors of RGCs are the pivotal reasons that inhibit ON regeneration and are closely linked with extrinsic factors. Intracellular cyclic adenosine monophosphate (cAMP) and calcium levels affect axon guidance and growth cone response to guidance molecules. Many genes, such as Bcl-2, PTEN, and mTOR, are crucial in cell proliferation, axon guidance, and growth during development, and play important roles in the regeneration and extension of RGC axons. With transgenic mice and related gene regulations, robust regeneration of RGC axons has been observed after ON injury in laboratories. Although various means of experimental treatments such as cell transplantation and gene therapy have achieved significant progress in neuronal survival, axonal regeneration, and restoration of the visual function after ON injury, many unresolved scientific problems still exist for their clinical applications. Therefore, we still need to overcome hurdles before developing effective therapy to treat optic neuropathy diseases in patients.
Persistent Identifierhttp://hdl.handle.net/10722/240216
ISSN
2023 Impact Factor: 3.1
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYou, SW-
dc.contributor.authorWu, MM-
dc.contributor.authorKuang, F-
dc.contributor.authorCho, KS-
dc.contributor.authorSo, KF-
dc.date.accessioned2017-04-19T08:21:22Z-
dc.date.available2017-04-19T08:21:22Z-
dc.date.issued2017-
dc.identifier.citationJournal of Neurorestoratology, 2017, v. 2017 n. 5, p. 59-72-
dc.identifier.issn2324-2426-
dc.identifier.urihttp://hdl.handle.net/10722/240216-
dc.description.abstractOptic neuropathy refers to disorders involving the optic nerve (ON). Any damage to ON or ON-deriving neurons, the retinal ganglion cells (RGCs), may lead to the breakdown of the optical signal transmission from the eye to the brain, thus resulting in a partial or complete vision loss. The causes of optic neuropathy include trauma, ischemia, inflammation, compression, infiltration, and mitochondrial damages. ON injuries include primary and secondary injuries. During these injury phases, various factors orchestrate injured axons to die back and become unable to regenerate, and these factors could be divided into two categories: extrinsic and intrinsic. Extrinsic inhibitory factors refer to the environmental conditions that influence the regeneration of injured axons. The presence of myelin inhibitors and glial scar, lack of neurotrophic factors, and inflammation mediated by injury are regarded as these extrinsic factors. Extrinsic factors need to trigger the intracellular signals to exert inhibitory effect. Proper regulation of these intracellular signals has been shown to be beneficial to ON regeneration. Intrinsic factors of RGCs are the pivotal reasons that inhibit ON regeneration and are closely linked with extrinsic factors. Intracellular cyclic adenosine monophosphate (cAMP) and calcium levels affect axon guidance and growth cone response to guidance molecules. Many genes, such as Bcl-2, PTEN, and mTOR, are crucial in cell proliferation, axon guidance, and growth during development, and play important roles in the regeneration and extension of RGC axons. With transgenic mice and related gene regulations, robust regeneration of RGC axons has been observed after ON injury in laboratories. Although various means of experimental treatments such as cell transplantation and gene therapy have achieved significant progress in neuronal survival, axonal regeneration, and restoration of the visual function after ON injury, many unresolved scientific problems still exist for their clinical applications. Therefore, we still need to overcome hurdles before developing effective therapy to treat optic neuropathy diseases in patients.-
dc.languageeng-
dc.publisherDove Medical Press Ltd.(DovePress). The Journal's web site is located at http://www.dovepress.com/journal-of-neurorestoratology-journal-
dc.relation.ispartofJournal of Neurorestoratology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleRestoration of optic neuropathy-
dc.typeArticle-
dc.identifier.emailSo, KF: hrmaskf@hku.hk-
dc.identifier.authoritySo, KF=rp00329-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.2147/JN.S120640-
dc.identifier.hkuros271912-
dc.identifier.volume2017-
dc.identifier.issue5-
dc.identifier.spage59-
dc.identifier.epage72-
dc.identifier.isiWOS:000396811000001-
dc.publisher.placeNew Zealand-
dc.identifier.issnl2324-2426-

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