Please use this identifier to cite or link to this item: https://doi.org/10.1155/2012/845698
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dc.titleThe diabetic heart: Too sweet for its own good?
dc.contributor.authorWhittington, H.J
dc.contributor.authorBabu, G.G
dc.contributor.authorMocanu, M.M
dc.contributor.authorYellon, D.M
dc.contributor.authorHausenloy, D.J
dc.date.accessioned2020-11-10T00:36:55Z
dc.date.available2020-11-10T00:36:55Z
dc.date.issued2012
dc.identifier.citationWhittington, H.J, Babu, G.G, Mocanu, M.M, Yellon, D.M, Hausenloy, D.J (2012). The diabetic heart: Too sweet for its own good?. Cardiology Research and Practice 1 (1) : 845698. ScholarBank@NUS Repository. https://doi.org/10.1155/2012/845698
dc.identifier.issn20900597
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/183236
dc.description.abstractDiabetes mellitus is a major risk factor for ischemic heart disease (IHD). Patients with diabetes and IHD experience worse clinical outcomes, suggesting that the diabetic heart may be more susceptible to ischemia-reperfusion injury (IRI). In contrast, the animal data suggests that the diabetic heart may be either more, equally, or even less susceptible to IRI. The conflicting animal data may be due to the choice of diabetic and/or IRI animal model. Ischemic conditioning, a phenomenon in which the heart is protected against IRI by one or more brief nonlethal periods of ischemia and reperfusion, may provide a novel cardioprotective strategy for the diabetic heart. Whether the diabetic heart is amenable to ischemic conditioning remains to be determined using relevant animal models of IRI and/or diabetes. In this paper, we review the limitations of the current experimental models used to investigate IRI and cardioprotection in the diabetic heart. © 2012 Hannah J. Whittington et al.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectalloxan
dc.subjectcaspase 3
dc.subjectcreatine kinase
dc.subjectG protein coupled receptor
dc.subjectglucokinase
dc.subjectglycogen synthase kinase 3beta
dc.subjectJanus kinase 2
dc.subjectnitric oxide synthase
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein bcl 2
dc.subjectprotein kinase B
dc.subjectprotein kinase C
dc.subjectreactive oxygen metabolite
dc.subjectstreptozocin
dc.subjectvasculotropin
dc.subjectage
dc.subjectapoptosis
dc.subjectcalcium cell level
dc.subjectcell survival
dc.subjectdiabetic cardiomyopathy
dc.subjectdisease predisposition
dc.subjectdyslipidemia
dc.subjectex vivo study
dc.subjectexperimental model
dc.subjectexperimental study
dc.subjectglucose tolerance
dc.subjectglucose transport
dc.subjectheart left ventricle function
dc.subjectheart muscle cell
dc.subjectheart protection
dc.subjectheart ventricle fibrillation
dc.subjecthyperglycemia
dc.subjecthypertension
dc.subjectin vitro study
dc.subjectin vivo study
dc.subjectinsulin dependent diabetes mellitus
dc.subjectischemic heart disease
dc.subjectischemic preconditioning
dc.subjectmitochondrial permeability
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectnonhuman
dc.subjectobesity
dc.subjectpancreas islet beta cell
dc.subjectpH
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectprotein phosphorylation
dc.subjectreperfusion injury
dc.subjectreview
dc.subjectsensitivity analysis
dc.subjectupregulation
dc.typeReview
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1155/2012/845698
dc.description.sourcetitleCardiology Research and Practice
dc.description.volume1
dc.description.issue1
dc.description.page845698
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