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Two types of mouse models for sarcopenia research: Senescence acceleration and genetic modification models

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dc.contributor.authorBaek, K.-W.-
dc.contributor.authorJung, Y.-K.-
dc.contributor.authorPark, J.S.-
dc.contributor.authorKim, J.-S.-
dc.contributor.authorHah, Y.-S.-
dc.contributor.authorKim, S.-J.-
dc.contributor.authorYoo, J.-I.-
dc.date.accessioned2022-12-26T12:01:07Z-
dc.date.available2022-12-26T12:01:07Z-
dc.date.issued2021-08-
dc.identifier.issn2287-6375-
dc.identifier.issn2287-7029-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/5634-
dc.description.abstractSarcopenia leads to loss of skeletal muscle mass, quality, and strength due to aging; it was recently given a disease code (International Classification of Diseases, Tenth Revision, Clinical Modification, M62.84). As a result, in recent years, sarcopenia-related research has increased. In addition, various studies seeking to prevent and treat sarcopenia by identifying the various mechanisms related to the reduction of skeletal muscle properties have been conducted. Previous studies have identified muscle synthesis and breakdown; investigating them has generated evidence for preventing and treating sarcopenia. Mouse models are still the most useful ones for determining mechanisms underlying sarcopenia through correlations and interventions involving specific genes and their phenotypes. Mouse models used to study sarcopenia often induce muscle atrophy by hindlimb unloading, denervation, or immobilization. Though it is less frequently used, the senescence-accelerated mouse can also be useful for sarcopenia research. Herein, we discuss cases where senescence-accelerated and genetically engineered mouse models were used in sarcopenia research and different perspectives to use them. ? 2021 The Korean Society for Bone and Mineral Research-
dc.format.extent13-
dc.language영어-
dc.language.isoENG-
dc.publisherKorean Society for Bone and Mineral Research-
dc.titleTwo types of mouse models for sarcopenia research: Senescence acceleration and genetic modification models-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.11005/JBM.2021.28.3.179-
dc.identifier.scopusid2-s2.0-85115286969-
dc.identifier.bibliographicCitationJournal of Bone Metabolism, v.28, no.3, pp 179 - 191-
dc.citation.titleJournal of Bone Metabolism-
dc.citation.volume28-
dc.citation.number3-
dc.citation.startPage179-
dc.citation.endPage191-
dc.type.docTypeReview-
dc.identifier.kciidART002752500-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.subject.keywordAuthorAging-
dc.subject.keywordAuthorMice-
dc.subject.keywordAuthorMuscle-
dc.subject.keywordAuthorSarcopenia-
dc.subject.keywordAuthorSkeletal-
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