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Article: (iv) Genetics of disc degeneration

Title(iv) Genetics of disc degeneration
Authors
KeywordsGenes
Genetics
Genomics
Intervertebral disc Degeneration
Mutations
Spine
Issue Date2008
PublisherChurchill Livingstone. The Journal's web site is located at http://www.elsevier.com/locate/cuor
Citation
Current Orthopaedics, 2008, v. 22 n. 4, p. 259-266 How to Cite?
AbstractLow back pain from Degenerative Disc Disease (DDD) is a common disorder, affecting quality of life and presenting a significant burden to industrialized societies. While DDD has been attributed to the accumulation of environmental factors imposed on the "normal" aging changes, studies have shown that the effects are modest. In fact, twin and familial aggregation studies have indicated a significant genetic contribution. Indeed, this is supported by the subsequent identification of genetic risk factors for DDD such as Vitamin D Receptor (VDR), Collagen IX (COL9A2 and COL9A3), collagen XI (COL11A1), Aggrecan (AGC1), Cartilage Intermediate Layer Protein (CILP), Asporin (ASPN) and Matrix MetalloProteinases (MMP2 and MMP3). A significant number of these are ExtraCellular Matrix (ECM) components of the disc, or genes that modulate their function. This review discusses the findings from the perspective of biological processes, which suggests that ECM homeostasis is important for proper disc function. © 2008 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/68005
ISSN
2008 Impact Factor: 0.288
ISI Accession Number ID
Funding AgencyGrant Number
Area of Excellence Award on Developmental Genomics and Skeletal ResearchAoE/M-04/04
Funding Information:

Some of the work described in this manuscript was partially supported by grants from the Area of Excellence Award on Developmental Genomics and Skeletal Research (AoE/M-04/04). The authors thank Deepa Natarajan for her help in editing the manuscripts.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorSong, YQen_HK
dc.contributor.authorSham, Pen_HK
dc.contributor.authorCheung, KMCen_HK
dc.contributor.authorChan, Den_HK
dc.date.accessioned2010-09-06T06:00:25Z-
dc.date.available2010-09-06T06:00:25Z-
dc.date.issued2008en_HK
dc.identifier.citationCurrent Orthopaedics, 2008, v. 22 n. 4, p. 259-266en_HK
dc.identifier.issn0268-0890en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68005-
dc.description.abstractLow back pain from Degenerative Disc Disease (DDD) is a common disorder, affecting quality of life and presenting a significant burden to industrialized societies. While DDD has been attributed to the accumulation of environmental factors imposed on the "normal" aging changes, studies have shown that the effects are modest. In fact, twin and familial aggregation studies have indicated a significant genetic contribution. Indeed, this is supported by the subsequent identification of genetic risk factors for DDD such as Vitamin D Receptor (VDR), Collagen IX (COL9A2 and COL9A3), collagen XI (COL11A1), Aggrecan (AGC1), Cartilage Intermediate Layer Protein (CILP), Asporin (ASPN) and Matrix MetalloProteinases (MMP2 and MMP3). A significant number of these are ExtraCellular Matrix (ECM) components of the disc, or genes that modulate their function. This review discusses the findings from the perspective of biological processes, which suggests that ECM homeostasis is important for proper disc function. © 2008 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherChurchill Livingstone. The Journal's web site is located at http://www.elsevier.com/locate/cuoren_HK
dc.relation.ispartofCurrent Orthopaedicsen_HK
dc.subjectGenesen_HK
dc.subjectGeneticsen_HK
dc.subjectGenomicsen_HK
dc.subjectIntervertebral disc Degenerationen_HK
dc.subjectMutationsen_HK
dc.subjectSpineen_HK
dc.title(iv) Genetics of disc degenerationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0268-0890&volume=22&issue=4&spage=259&epage=266 &date=2008&atitle=Genetics+of+disc+degenerationen_HK
dc.identifier.emailSong, YQ: songy@hku.hken_HK
dc.identifier.emailSham, P: pcsham@hku.hken_HK
dc.identifier.emailCheung, KMC: cheungmc@hku.hken_HK
dc.identifier.emailChan, D: chand@hku.hken_HK
dc.identifier.authoritySong, YQ=rp00488en_HK
dc.identifier.authoritySham, P=rp00459en_HK
dc.identifier.authorityCheung, KMC=rp00387en_HK
dc.identifier.authorityChan, D=rp00540en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cuor.2008.05.007en_HK
dc.identifier.scopuseid_2-s2.0-51249114770en_HK
dc.identifier.hkuros154522en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-51249114770&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume22en_HK
dc.identifier.issue4en_HK
dc.identifier.spage259en_HK
dc.identifier.epage266en_HK
dc.identifier.isiWOS:000260098200004-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.projectDevelopmental genomics and skeletal research-
dc.identifier.scopusauthoridSong, YQ=7404921212en_HK
dc.identifier.scopusauthoridSham, P=34573429300en_HK
dc.identifier.scopusauthoridCheung, KMC=7402406754en_HK
dc.identifier.scopusauthoridChan, D=7402216545en_HK

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