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dc.contributor.authorElkasrawy, Moataz N.
dc.date.accessioned2014-05-29T21:29:34Z
dc.date.available2014-05-29T21:29:34Z
dc.date.issued2010-11en
dc.identifier.urihttp://hdl.handle.net/10675.2/317633
dc.descriptionThe file you are attempting to access is currently restricted to Augusta University. Please log in with your NetID if off campus.
dc.description.abstractTraumatic musculoskeletal injuries frequently include damage to both muscle and bone where muscle injury itself can delay bone healing. Myostatin (GDF-8) is a member of the transforming growth factor-β (TGF-β) superfamily, and a negative regulator of skeletal muscle growth. Loss of myostatin function leads to a doubling of skeletal muscle mass, a general increase in bone density, and an increase in fracture callus bone volume. Myostatin is highly expressed during the first twenty-four hours after fracture, yet nothing is known about its role in fracture repair. We hypothesize that myostatin is a key regulator in the process of bone regeneration, and is a major therapeutic target for enhancement of fracture healing. Pharmacological inhibition of myostatin may therefore improve the regenerative capacity of both muscle and bone.
dc.language.isoen_USen
dc.relation.urlhttp://search.proquest.com/docview/822626277?accountid=12365en
dc.subjectMyostatinen
dc.subjectGDF-8en
dc.subjecttransforming growth factor-βen
dc.subjectTGF-βen
dc.subjectskeletal muscle growthen
dc.subjectbone fractureen
dc.subjectRegenerationen
dc.titleThe Role of Myostatin (GDF-8) in Chondrogenesis and Fracture Healingen
dc.typeDissertationen
dc.contributor.departmentDepartment of Medicineen
dc.description.advisorHamrick, Marken
dc.description.degreeDoctor of Philosophy (Ph.D.)en
dc.description.committeeBollag, Wendy; Borke, James; Hill, William; Isales, Carlosen
refterms.dateFOA2020-10-15T13:54:32Z
html.description.abstractTraumatic musculoskeletal injuries frequently include damage to both muscle and bone where muscle injury itself can delay bone healing. Myostatin (GDF-8) is a member of the transforming growth factor-β (TGF-β) superfamily, and a negative regulator of skeletal muscle growth. Loss of myostatin function leads to a doubling of skeletal muscle mass, a general increase in bone density, and an increase in fracture callus bone volume. Myostatin is highly expressed during the first twenty-four hours after fracture, yet nothing is known about its role in fracture repair. We hypothesize that myostatin is a key regulator in the process of bone regeneration, and is a major therapeutic target for enhancement of fracture healing. Pharmacological inhibition of myostatin may therefore improve the regenerative capacity of both muscle and bone.


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