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dc.contributor.authorCraige, Siobhan M.
dc.contributor.authorChen, Kai
dc.contributor.authorBlanton, Robert M.
dc.contributor.authorKeaney, John F.
dc.contributor.authorKant, Shashi
dc.date.accessioned2020-01-14T15:19:59Z
dc.date.available2020-01-14T15:19:59Z
dc.date.issued2019-07-19
dc.identifierARTN BSR20190267 (Article number)
dc.identifier.issn0144-8463
dc.identifier.otherBSR20190267 (PII)
dc.identifier.urihttp://hdl.handle.net/10919/96428
dc.description.abstractCardiometabolic syndrome (CMS) describes the cluster of metabolic and cardiovascular diseases that are generally characterized by impaired glucose tolerance, intra-abdominal adiposity, dyslipidemia, and hypertension. CMS currently affects more than 25% of the world's population and the rates of diseases are rapidly rising. These CMS conditions represent critical risk factors for cardiovascular diseases including atherosclerosis, heart failure, myocardial infarction, and peripheral artery disease (PAD). Therefore, it is imperative to elucidate the underlying signaling involved in disease onset and progression. The c-Jun N-terminal Kinases (JNKs) are a family of stress signaling kinases that have been recently indicated in CMS. The purpose of this review is to examine the in vivo implications of JNK as a potential therapeutic target for CMS. As the constellation of diseases associated with CMS are complex and involve multiple tissues and environmental triggers, carefully examining what is known about the JNK pathway will be important for specificity in treatment strategies.en
dc.format.extent18 page(s)
dc.format.mediumElectronic-Print
dc.languageEnglish
dc.publisherPortland Press
dc.relation.urihttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000476477700001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=930d57c9ac61a043676db62af60056c1
dc.rightsCreative Commons Attribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectBiochemistry & Molecular Biology
dc.subjectCell Biology
dc.subjectACTIVATED PROTEIN-KINASES
dc.subjectJUN NH2-TERMINAL KINASE
dc.subjectJIP1 SCAFFOLD PROTEIN
dc.subjectN-TERMINAL KINASES
dc.subjectCARDIAC-HYPERTROPHY
dc.subjectINSULIN-RESISTANCE
dc.subjectMAP KINASE
dc.subjectENDOTHELIAL DYSFUNCTION
dc.subjectSIGNAL-TRANSDUCTION
dc.subjectFATTY-ACIDS
dc.subjectSignaling
dc.subjectcardiovascular disease
dc.subjectmetabolic regulation
dc.subjectBiochemistry & Molecular Biology
dc.subject0601 Biochemistry and Cell Biology
dc.titleJNK and cardiometabolic dysfunctionen
dc.typeArticle - Refereed
dc.date.updated2020-01-14T15:19:55Z
dc.description.versionPublished (Publication status)
dc.contributor.departmentHuman Nutrition, Foods, and Exerciseen_US
dc.title.serialBioscience Reportsen
dc.identifier.doihttps://doi.org/10.1042/BSR20190267
dc.type.otherJournal
dc.identifier.volume39
dc.identifier.issue7
dc.identifier.pmid31270248
dcterms.dateAccepted2019-07-02
dc.identifier.eissn1573-4935
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences
pubs.organisational-group/Virginia Tech/Faculty of Health Sciences
pubs.organisational-group/Virginia Tech/All T&R Faculty
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences/Human Nutrition, Foods, & Exercise
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences/CALS T&R Faculty
pubs.organisational-group/Virginia Tech


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Creative Commons Attribution 4.0 International
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