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Article: Mechanisms of secondary degeneration after partial optic nerve transection
Title | Mechanisms of secondary degeneration after partial optic nerve transection |
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Authors | |
Keywords | secondary degeneration partial injury optic nerve oxidative stress excitotoxicity |
Issue Date | 2014 |
Publisher | Medknow Publications and Media Pvt. Ltd. The Journal's web site is located at http://www.nrronline.org/ |
Citation | Neural Regeneration Research, 2014, v. 9 n. 6, p. 565-574 How to Cite? |
Abstract | Secondary degeneration occurs commonly in the central nervous system after traumatic injuries and following acute and chronic diseases, including glaucoma. A constellation of mechanisms have been shown to be associated with secondary degeneration including apoptosis, necrosis, autophagy, oxidative stress, excitotoxicity, derangements in ionic homeostasis and calcium influx. Glial cells, such as microglia, astrocytes and oligodendrocytes, have also been demonstrated to take part in the process of secondary injury. Partial optic nerve transection is a useful model which was established about 13 years ago. The merit of this model compared with other optic nerve injury models used for glaucoma study, including complete optic nerve transection model and optic nerve crush model, is the possibility to separate primary degeneration from secondary degeneration in location. Therefore, it provides a good tool for the study of secondary degeneration. This review will focus on the research progress of the mechanisms of secondary degeneration using partial optic nerve transection model. |
Persistent Identifier | http://hdl.handle.net/10722/206189 |
ISSN | 2023 Impact Factor: 5.9 2023 SCImago Journal Rankings: 0.967 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Li, H | - |
dc.contributor.author | Ruan, Y | - |
dc.contributor.author | Ren, C | - |
dc.contributor.author | Cui, Q | - |
dc.contributor.author | So, KF | - |
dc.date.accessioned | 2014-10-20T14:01:01Z | - |
dc.date.available | 2014-10-20T14:01:01Z | - |
dc.date.issued | 2014 | - |
dc.identifier.citation | Neural Regeneration Research, 2014, v. 9 n. 6, p. 565-574 | - |
dc.identifier.issn | 1673-5374 | - |
dc.identifier.uri | http://hdl.handle.net/10722/206189 | - |
dc.description.abstract | Secondary degeneration occurs commonly in the central nervous system after traumatic injuries and following acute and chronic diseases, including glaucoma. A constellation of mechanisms have been shown to be associated with secondary degeneration including apoptosis, necrosis, autophagy, oxidative stress, excitotoxicity, derangements in ionic homeostasis and calcium influx. Glial cells, such as microglia, astrocytes and oligodendrocytes, have also been demonstrated to take part in the process of secondary injury. Partial optic nerve transection is a useful model which was established about 13 years ago. The merit of this model compared with other optic nerve injury models used for glaucoma study, including complete optic nerve transection model and optic nerve crush model, is the possibility to separate primary degeneration from secondary degeneration in location. Therefore, it provides a good tool for the study of secondary degeneration. This review will focus on the research progress of the mechanisms of secondary degeneration using partial optic nerve transection model. | - |
dc.language | eng | - |
dc.publisher | Medknow Publications and Media Pvt. Ltd. The Journal's web site is located at http://www.nrronline.org/ | - |
dc.relation.ispartof | Neural Regeneration Research | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | secondary degeneration | - |
dc.subject | partial injury | - |
dc.subject | optic nerve | - |
dc.subject | oxidative stress | - |
dc.subject | excitotoxicity | - |
dc.title | Mechanisms of secondary degeneration after partial optic nerve transection | - |
dc.type | Article | - |
dc.identifier.email | Li, H: lhy2012@hku.hk | - |
dc.identifier.email | So, KF: hrmaskf@hku.hk | - |
dc.identifier.authority | So, KF=rp00329 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.4103/1673-5374.130093 | - |
dc.identifier.pmid | 25206855 | - |
dc.identifier.pmcid | PMC4146235 | - |
dc.identifier.scopus | eid_2-s2.0-84901018689 | - |
dc.identifier.hkuros | 241292 | - |
dc.identifier.volume | 9 | - |
dc.identifier.issue | 6 | - |
dc.identifier.spage | 565 | - |
dc.identifier.epage | 574 | - |
dc.identifier.isi | WOS:000334324200001 | - |
dc.publisher.place | China | - |
dc.identifier.issnl | 1673-5374 | - |