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dc.contributor.authorHummasti, Sarah
dc.contributor.authorHotamisligil, Gokhan
dc.date.accessioned2019-08-19T11:16:23Z
dc.date.issued2010-09-03
dc.identifier.citationHummasti, Sarah, and Gökhan S. Hotamisligil. 2010. “Endoplasmic Reticulum Stress and Inflammation in Obesity and Diabetes.” Circulation Research 107 (5): 579–91. https://doi.org/10.1161/circresaha.110.225698.en_US
dc.identifier.issn0009-7330en_US
dc.identifier.issn1524-4571en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:41200930*
dc.description.abstractObesity is a major problem worldwide that increases risk for a wide range of diseases, including diabetes and heart disease. As such, it is increasingly important to understand how excess adiposity can perturb normal metabolic functions. It is now clear that this disruption involves not only pathways controlling lipid and glucose homeostasis but also integration of metabolic and immune response pathways. Under conditions of nutritional excess, this integration can result in a metabolically driven, low-grade, chronic inflammatory state, referred to as "metaflammation," that targets metabolically critical organs and tissues to adversely affect systemic homeostasis. Endoplasmic reticulum dysfunction is another important feature of chronic metabolic disease that is also linked to both metabolic and immune regulation. A thorough understanding of how these pathways intersect to maintain metabolic homeostasis, as well as how this integration is altered under conditions of nutrient excess, is important to fully understand, and subsequently treat, chronic metabolic diseases.en_US
dc.language.isoen_USen_US
dc.publisherOvid Technologies (Wolters Kluwer Health)en_US
dash.licenseMETA_ONLY
dc.subjectPhysiologyen_US
dc.subjectCardiology and Cardiovascular Medicineen_US
dc.titleEndoplasmic Reticulum Stress and Inflammation in Obesity and Diabetesen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalCirculation Researchen_US
dash.depositing.authorHotamisligil, Gokhan
dc.date.available2019-08-19T11:16:23Z
dash.workflow.comments1Science Serial ID 21699en_US
dc.identifier.doi10.1161/circresaha.110.225698
dc.source.journalCirc Res
dash.source.volume107;5
dash.source.page579-591
dash.contributor.affiliatedHotamisligil, Gokhan


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