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Conference Paper: Mesenchymal stem cells mediate disk regeneration by suppression of fibrosis in nucleus pulposus

TitleMesenchymal stem cells mediate disk regeneration by suppression of fibrosis in nucleus pulposus
Authors
Leung, VYLAladin, DMLv, FTam, VSun, YLu, WWWu, EXLuk, KDKChan, DCheung, KMC
Issue Date2012
PublisherGeorg Thieme Verlag. The Journal's web site is located at http://www.thieme.com/index.php?page=shop.product_details&flypage=flypage.tpl&product_id=1351&category_id=90&option=com_virtuemart&Itemid=53
Citation
The 2012 World Forum for Spine Research (WFSR): The Intervertebral Disc - from Degeneration to Pain, Helsinki, Finland, 18-21 June 2012. In Global Spine Journal, 2012, v. 2 n. S1, no. S4.06 How to Cite?
DOI: http://dx.doi.org/10.1055/s-0032-1319877
AbstractINTRODUCTION: Confluent fibrosis, manifested as over-accumulation of fibrous matrix during tissue repair or remodeling, leads to scar formation and often organ failure. Studies suggest that 68% of protruded intervertebral disks and 44% of prolapsed IVD exhibit signs of fibrosis in the nucleus pulposus (NP) and that disk scarring indicates advanced stages of degeneration. It is not clear how fibrosis contributes to the initiation or progression of disk degeneration, and conversely if the prevention of fibrotic events plays a role in IVD repair or regeneration. Mesenchymal stem cells (MSCs) may arrest IVD degeneration and cross-talk with IVD cells via cell-cell contact or long-range signaling, implying MSCs may modulate disk microenvironment and function indirectly. Lup...
DescriptionOral Presentations: S4.06
Persistent Identifierhttp://hdl.handle.net/10722/153100
ISSN
2192-5682
2023 Impact Factor: 2.6
2023 SCImago Journal Rankings: 1.264

 

DC FieldValueLanguage
dc.contributor.authorLeung, VYLen_US
dc.contributor.authorAladin, DM-
dc.contributor.authorLv, F-
dc.contributor.authorTam, V-
dc.contributor.authorSun, Y-
dc.contributor.authorLu, WW-
dc.contributor.authorWu, EX-
dc.contributor.authorLuk, KDK-
dc.contributor.authorChan, D-
dc.contributor.authorCheung, KMC-
dc.date.accessioned2012-07-16T09:56:38Z-
dc.date.available2012-07-16T09:56:38Z-
dc.date.issued2012en_US
dc.identifier.citationThe 2012 World Forum for Spine Research (WFSR): The Intervertebral Disc - from Degeneration to Pain, Helsinki, Finland, 18-21 June 2012. In Global Spine Journal, 2012, v. 2 n. S1, no. S4.06en_US
dc.identifier.issn2192-5682-
dc.identifier.urihttp://hdl.handle.net/10722/153100-
dc.descriptionOral Presentations: S4.06-
dc.description.abstractINTRODUCTION: Confluent fibrosis, manifested as over-accumulation of fibrous matrix during tissue repair or remodeling, leads to scar formation and often organ failure. Studies suggest that 68% of protruded intervertebral disks and 44% of prolapsed IVD exhibit signs of fibrosis in the nucleus pulposus (NP) and that disk scarring indicates advanced stages of degeneration. It is not clear how fibrosis contributes to the initiation or progression of disk degeneration, and conversely if the prevention of fibrotic events plays a role in IVD repair or regeneration. Mesenchymal stem cells (MSCs) may arrest IVD degeneration and cross-talk with IVD cells via cell-cell contact or long-range signaling, implying MSCs may modulate disk microenvironment and function indirectly. Lup...-
dc.languageengen_US
dc.publisherGeorg Thieme Verlag. The Journal's web site is located at http://www.thieme.com/index.php?page=shop.product_details&flypage=flypage.tpl&product_id=1351&category_id=90&option=com_virtuemart&Itemid=53-
dc.relation.ispartofGlobal Spine Journalen_US
dc.rightsGlobal Spine Journal. Copyright © Georg Thieme Verlag.-
dc.titleMesenchymal stem cells mediate disk regeneration by suppression of fibrosis in nucleus pulposusen_US
dc.typeConference_Paperen_US
dc.identifier.emailLeung, VYL: vicleung@hku.hken_US
dc.identifier.emailAladin, DM: darwesh@hkucc.hku.hk-
dc.identifier.emailLv, F: h0794164@hku.hk-
dc.identifier.emailTam, V: vivtam@hku.hk-
dc.identifier.emailSun, Y: hkusunyi@HKUSUC.hku.hk-
dc.identifier.emailLu, WW: wwlu@hku.hk-
dc.identifier.emailWu, EX: ewu1@hkucc.hku.hk-
dc.identifier.emailLuk, KDK: hcm21000@hku.hk-
dc.identifier.emailChan, D: chand@hku.hk-
dc.identifier.emailCheung, KMC: cheungmc@hku.hk-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1055/s-0032-1319877-
dc.identifier.hkuros200698en_US
dc.identifier.hkuros234851-
dc.identifier.volume2-
dc.identifier.issuesuppl. 1-
dc.publisher.placeGermany-
dc.identifier.issnl2192-5682-

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