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Article: Mechanisms of secondary degeneration after partial optic nerve transection

TitleMechanisms of secondary degeneration after partial optic nerve transection
Authors
Keywordssecondary degeneration
partial injury
optic nerve
oxidative stress
excitotoxicity
Issue Date2014
PublisherMedknow 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?
AbstractSecondary 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 Identifierhttp://hdl.handle.net/10722/206189
ISSN
2019 Impact Factor: 3.171
2015 SCImago Journal Rankings: 0.337
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, H-
dc.contributor.authorRuan, Y-
dc.contributor.authorRen, C-
dc.contributor.authorCui, Q-
dc.contributor.authorSo, KF-
dc.date.accessioned2014-10-20T14:01:01Z-
dc.date.available2014-10-20T14:01:01Z-
dc.date.issued2014-
dc.identifier.citationNeural Regeneration Research, 2014, v. 9 n. 6, p. 565-574-
dc.identifier.issn1673-5374-
dc.identifier.urihttp://hdl.handle.net/10722/206189-
dc.description.abstractSecondary 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.languageeng-
dc.publisherMedknow Publications and Media Pvt. Ltd. The Journal's web site is located at http://www.nrronline.org/-
dc.relation.ispartofNeural Regeneration Research-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectsecondary degeneration-
dc.subjectpartial injury-
dc.subjectoptic nerve-
dc.subjectoxidative stress-
dc.subjectexcitotoxicity-
dc.titleMechanisms of secondary degeneration after partial optic nerve transection-
dc.typeArticle-
dc.identifier.emailLi, H: lhy2012@hku.hk-
dc.identifier.emailSo, KF: hrmaskf@hku.hk-
dc.identifier.authoritySo, KF=rp00329-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.4103/1673-5374.130093-
dc.identifier.pmid25206855-
dc.identifier.pmcidPMC4146235-
dc.identifier.scopuseid_2-s2.0-84901018689-
dc.identifier.hkuros241292-
dc.identifier.volume9-
dc.identifier.issue6-
dc.identifier.spage565-
dc.identifier.epage574-
dc.identifier.isiWOS:000334324200001-
dc.publisher.placeChina-

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