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Skeletal Class III phenotype: link between animal models and human genetics: a scoping review

dc.contributor.authorDehesa‐Santos, Alexandra
dc.contributor.authorFaria-Teixeira, Maria Cristina
dc.contributor.authorIglesias‐Linares, Alejandro
dc.date.accessioned2024-01-09T14:46:13Z
dc.date.available2024-01-09T14:46:13Z
dc.date.issued2023
dc.description© 2023 The Authors. Journal of Experimental Zoology Part B: Molecular and Developmental Evolution published by Wiley Periodicals LLC.This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.pt_PT
dc.description.abstractThis study aimed to identify evidence from animal studies examining genetic variants underlying maxillomandibular discrepancies resulting in a skeletal Class III (SCIII) malocclusion phenotype. Following the Manual for Evidence Synthesis of the JBI and the PRISMA extension for scoping reviews, a participant, concept, context question was formulated and systematic searches were executed in the PubMed, Scopus, WOS, Scielo, Open Gray, and Mednar databases. Of the 779 identified studies, 13 met the selection criteria and were included in the data extraction. The SCIII malocclusion phenotype was described as mandibular prognathism in the Danio rerio, Dicentrarchus labrax, and Equus africanus asinus models; and as maxillary deficiency in the Felis silvestris catus, Canis familiaris, Salmo trutta, and Mus musculus models. The identified genetic variants highlight the significance of BMP and TGF-β signaling. Their regulatory pathways and genetic interactions link them to cellular bone regulation events, particularly ossification regulation of postnatal cranial synchondroses. In conclusion, twenty genetic variants associated with the skeletal SCIII malocclusion phenotype were identified in animal models. Their interactions and regulatory pathways corroborate the role of these variants in bone growth, differentiation events, and ossification regulation of postnatal cranial synchondroses.pt_PT
dc.description.sponsorshipThis study was conducted under a pre‐doctoral contract for research personnel in training (CT63/19‐CT64/19). This study was funded by the Complutense University of Madrid and Banco Santander.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationJ Exp Zool B Mol Dev Evol. 2024 Jan;342(1):21-44pt_PT
dc.identifier.doi10.1002/jez.b.23230pt_PT
dc.identifier.eissn1552-5015
dc.identifier.issn1552-5007
dc.identifier.urihttp://hdl.handle.net/10451/61665
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherWileypt_PT
dc.relation.publisherversionhttps://onlinelibrary.wiley.com/journal/15525015pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectAnimal modelpt_PT
dc.subjectGenetic variantspt_PT
dc.subjectMandibular prognathismpt_PT
dc.subjectMaxillary deficiencypt_PT
dc.subjectSkeletal Class III malocclusion phenotypept_PT
dc.titleSkeletal Class III phenotype: link between animal models and human genetics: a scoping reviewpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage44pt_PT
oaire.citation.issue1pt_PT
oaire.citation.startPage21pt_PT
oaire.citation.titleJournal of Experimental Zoology Part B: Molecular and Developmental Evolution (JEZ-B)pt_PT
oaire.citation.volume342pt_PT
person.identifier.ciencia-id3C10-E25B-FBE4
person.identifier.orcid0000-0002-4707-0773
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicatione85df547-cb07-4038-9a08-3a90a2ef4810
relation.isAuthorOfPublication.latestForDiscoverye85df547-cb07-4038-9a08-3a90a2ef4810

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