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dc.contributor.authorApostolova, Nadezda-
dc.contributor.authorIannantuoni, Francesca-
dc.contributor.authorGruevska, Aleksandra-
dc.contributor.authorMuntané, Jordi-
dc.contributor.authorRocha, Milagros-
dc.contributor.authorVictor, Víctor M.-
dc.date.accessioned2021-02-26T13:40:29Z-
dc.date.available2021-02-26T13:40:29Z-
dc.date.issued2020-07-
dc.identifierdoi: 10.1016/j.redox.2020.101517-
dc.identifiere-issn: 2213-2317-
dc.identifier.citationRedox Biology 34: 101517 (2020)-
dc.identifier.urihttp://hdl.handle.net/10261/230875-
dc.description.abstractType 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin is still not fully understood. This review provides an overview of the existing literature concerning the beneficial mitochondrial and vascular effects of metformin, which it exerts by diminishing oxidative stress and reducing leukocyte-endothelium interactions. Specifically, we describe the molecular mechanisms involved in metformin's effect on gluconeogenesis, its capacity to interfere with major metabolic pathways (AMPK and mTORC1), its action on mitochondria and its antioxidant effects. We also discuss potential targets for therapeutic intervention based on these molecular actions.-
dc.description.sponsorshipThis work was funded by grants PI16/00090, PI19/00838, PI19/0437,PI19/01266 and CIBERehd CB06/04/0071 by Carlos III Health Institute and by the European Regional Development Fund (ERDF ‘‘A way to build Europe’‘); by PROMETEO/2019/027 by Ministry of Education of the Valencian Regional Government; by RTI2018-096748-B-100 (Spanish Ministry of Science, Innovation and Universities), by Andalusian Ministry of Economy, Innovation, Science and Employment (CTS-6264), Andalusian Ministry of Equality, Health and Social Policies (PI-0198-2016) and by an unrestricted grant from Menarini S.A. M.R and VM.V are recipients of contracts from the Ministry of Health of the Valencian Regional Government and Carlos III Health Institute (CPII16/00037 and CES10/030, respectively) while AG is supported by the Foundation “Juan Esplugues”.-
dc.languageeng-
dc.publisherElsevier-
dc.relationMICIU/ICTI2017-2020/RTI2018-096748-B-100-
dc.relation.isversionofPublisher's version-
dc.rightsopenAccess-
dc.subjectType 2 diabetes-
dc.subjectMetformin-
dc.subjectOxidative stress-
dc.subjectPathophysiology-
dc.subjectTreatment-
dc.subjectAtherosclerosis-
dc.subjectMitochondria-
dc.titleMechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions-
dc.typeartículo de revisión-
dc.relation.publisherversionhttp://doi.org/10.1016/j.redox.2020.101517-
dc.date.updated2021-02-26T13:40:30Z-
dc.rights.licensehttps://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.contributor.funderCentro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas (España)-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderEuropean Commission-
dc.contributor.funderGeneralitat Valenciana-
dc.contributor.funderMinisterio de Ciencia, Innovación y Universidades (España)-
dc.contributor.funderAgencia Estatal de Investigación (España)-
dc.contributor.funderJunta de Andalucía-
dc.contributor.funderGrupo Menarini-
dc.contributor.funderFundación Juan Esplugues-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100011033es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003359es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100011011es_ES
dc.type.coarhttp://purl.org/coar/resource_type/c_dcae04bces_ES
item.grantfulltextopen-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextWith Fulltext-
item.openairetypeartículo de revisión-
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