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dc.contributor.authorWalsh, David A
dc.date.accessioned2022-05-31T13:33:59Z
dc.date.available2022-05-31T13:33:59Z
dc.date.issued2012-05
dc.identifier.citationMapp, P. I. and Walsh, D. A. (2012) ‘Mechanisms and targets of angiogenesis and nerve growth in osteoarthritis’, Nature Reviews Rheumatology, 8(7), p. 390en_US
dc.identifier.urihttp://hdl.handle.net/20.500.12904/15565
dc.description.abstractDuring osteoarthritis (OA), angiogenesis is increased in the synovium, osteophytes and menisci and leads to ossification in osteophytes and the deep layers of articular cartilage. Angiogenic and antiangiogenic factors might both be upregulated in the osteoarthritic joint; however, vascular growth predominates, and the articular cartilage loses its resistance to vascularization. In addition, blood vessel growth is increased at--and disrupts--the osteochondral junction. Angiogenesis in this location is dependent on the creation of channels from subchondral bone spaces into noncalcified articular cartilage. Inflammation drives synovial angiogenesis through macrophage activation. Blood vessel and nerve growth are linked by common pathways that involve the release of proangiogenic factors, such as vascular endothelial growth factor, β-nerve growth factor and neuropeptides. Proangiogenic factors might also stimulate nerve growth, and molecules produced by vascular cells could both stimulate and guide nerve growth. As sensory nerves grow along new blood vessels in osteoarthritic joints, they eventually penetrate noncalcified articular cartilage, osteophytes and the inner regions of menisci. Angiogenesis could, therefore, contribute to structural damage and pain in OA and provide potential targets for new treatments.
dc.description.urihttps://www.nature.com/articles/nrrheum.2012.80en_US
dc.publisherNature Reviews Rheumatologyen_US
dc.subjectResearchen_US
dc.subjectPhysiological aspectsen_US
dc.subjectNeovascularizationen_US
dc.subjectOsteoarthritisen_US
dc.subjectHomeostasisen_US
dc.titleMechanisms and targets of angiogenesis and nerve growth in osteoarthritis.en_US
dc.typeArticleen_US
rioxxterms.funderDefault funderen_US
rioxxterms.identifier.projectDefault projecten_US
rioxxterms.versionNAen_US
rioxxterms.versionofrecord10.1038/nrrheum.2012.80en_US
rioxxterms.typeJournal Article/Reviewen_US
refterms.panelUnspecifieden_US
html.description.abstractDuring osteoarthritis (OA), angiogenesis is increased in the synovium, osteophytes and menisci and leads to ossification in osteophytes and the deep layers of articular cartilage. Angiogenic and antiangiogenic factors might both be upregulated in the osteoarthritic joint; however, vascular growth predominates, and the articular cartilage loses its resistance to vascularization. In addition, blood vessel growth is increased at--and disrupts--the osteochondral junction. Angiogenesis in this location is dependent on the creation of channels from subchondral bone spaces into noncalcified articular cartilage. Inflammation drives synovial angiogenesis through macrophage activation. Blood vessel and nerve growth are linked by common pathways that involve the release of proangiogenic factors, such as vascular endothelial growth factor, β-nerve growth factor and neuropeptides. Proangiogenic factors might also stimulate nerve growth, and molecules produced by vascular cells could both stimulate and guide nerve growth. As sensory nerves grow along new blood vessels in osteoarthritic joints, they eventually penetrate noncalcified articular cartilage, osteophytes and the inner regions of menisci. Angiogenesis could, therefore, contribute to structural damage and pain in OA and provide potential targets for new treatments.en_US
rioxxterms.funder.project94a427429a5bcfef7dd04c33360d80cden_US


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