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dc.contributor.authorGero, Domokos
dc.date.accessioned2021-06-02T10:10:43Z
dc.date.available2021-06-02T10:10:43Z
dc.date.issued2018
dc.identifierONIX_20210602_10.5772/intechopen.71433_371
dc.identifier.urihttps://library.oapen.org/handle/20.500.12657/49257
dc.description.abstractGlucose-induced endothelial dysfunction plays a fundamental role in the development of diabetic vascular complications and glycemic control (the foundation of diabetes care) provides limited protection against the cardiovascular complications. Therefore, identification of novel drug targets and treatment approaches for diabetes complications represent a key direction of current pharmaceutical research. The “unifying theory” of hyperglycemia-induced endothelial cell injury organizes the events of cellular dysfunction in a linear cascade and identifies mitochondrial superoxide generation as the triggering event of the injury. Exposure to high glucose concentration for long periods or repeated glycemic swings may induce changes in metabolic substrate availability and lead to mitochondrial hyperpolarization. Changes in the mitochondrial membrane potential induce superoxide production by the electron transport chain and result in oxidative stress. Mitochondrial superoxide is also responsible for the induction of other sources of reactive oxygen species (ROS) within the cells, including advanced glycation end products (AGEs) and the NADPH oxidase. Mitochondria also show morphological changes and impaired assembly of the respiratory complexes occurs, which results in cellular energy failure, cell senescence and vascular dysfunction. Current intervention strategies aim to inhibit the mitochondrial ROS production and novel therapeutic approaches are expected to provide valuable tools in diabetes therapy in the upcoming years.
dc.languageEnglish
dc.subject.classificationbic Book Industry Communication::M Medicine::MJ Clinical & internal medicine::MJD Cardiovascular medicine
dc.subject.otherhyperglycemia, diabetes, endothelial cells, oxidative stress, mitochondria, electron transport chain, superoxide, bioenergetics
dc.titleChapter Hyperglycemia-Induced Endothelial Dysfunction
dc.typechapter
oapen.identifier.doi10.5772/intechopen.71433
oapen.relation.isPublishedBy09f6769d-48ed-467d-b150-4cf2680656a1
oapen.relation.isFundedByFP7-PEOPLE-2013-IEF
oapen.grant.number628100
oapen.grant.acronymH2S IN DIABETES


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