JNK and cardiometabolic dysfunction

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dc.contributor.authorCraige, Siobhan M.en
dc.contributor.authorChen, Kaien
dc.contributor.authorBlanton, Robert M.en
dc.contributor.authorKeaney, John F.en
dc.contributor.authorKant, Shashien
dc.contributor.departmentHuman Nutrition, Foods, and Exerciseen
dc.date.accessioned2020-01-14T15:19:59Zen
dc.date.available2020-01-14T15:19:59Zen
dc.date.issued2019-07-19en
dc.date.updated2020-01-14T15:19:55Zen
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.description.versionPublished (Publication status)en
dc.format.extent18 page(s)en
dc.format.mimetypeapplication/pdfen
dc.identifierARTN BSR20190267 (Article number)en
dc.identifier.doihttps://doi.org/10.1042/BSR20190267en
dc.identifier.eissn1573-4935en
dc.identifier.issn0144-8463en
dc.identifier.issue7en
dc.identifier.otherBSR20190267 (PII)en
dc.identifier.pmid31270248en
dc.identifier.urihttp://hdl.handle.net/10919/96428en
dc.identifier.volume39en
dc.language.isoenen
dc.publisherPortland Pressen
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=930d57c9ac61a043676db62af60056c1en
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectBiochemistry & Molecular Biologyen
dc.subjectCell Biologyen
dc.subjectACTIVATED PROTEIN-KINASESen
dc.subjectJUN NH2-TERMINAL KINASEen
dc.subjectJIP1 SCAFFOLD PROTEINen
dc.subjectN-TERMINAL KINASESen
dc.subjectCARDIAC-HYPERTROPHYen
dc.subjectINSULIN-RESISTANCEen
dc.subjectMAP KINASEen
dc.subjectENDOTHELIAL DYSFUNCTIONen
dc.subjectSIGNAL-TRANSDUCTIONen
dc.subjectFATTY-ACIDSen
dc.subjectSignalingen
dc.subjectcardiovascular diseaseen
dc.subjectmetabolic regulationen
dc.subject0601 Biochemistry and Cell Biologyen
dc.titleJNK and cardiometabolic dysfunctionen
dc.title.serialBioscience Reportsen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.otherJournalen
dcterms.dateAccepted2019-07-02en
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciencesen
pubs.organisational-group/Virginia Tech/Faculty of Health Sciencesen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences/Human Nutrition, Foods, & Exerciseen
pubs.organisational-group/Virginia Tech/Agriculture & Life Sciences/CALS T&R Facultyen
pubs.organisational-group/Virginia Techen

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