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dc.contributor.authorDíaz Morales, Noelia 
dc.contributor.authorRovira-Llopis, Susana
dc.contributor.authorBañuls, Celia
dc.contributor.authorEscribano-Lopez, Irene
dc.contributor.authorde Marañon, Arantxa Martinez
dc.contributor.authorLopez-Domenech, Sandra
dc.contributor.authorOrden, Samuel
dc.contributor.authorRoldan-Torres, Ildefonso
dc.contributor.authorAlvarez, Angeles
dc.contributor.authorVeses, Silvia
dc.contributor.authorJover, Ana
dc.contributor.authorRocha, Milagros
dc.contributor.authorHernandez-Mijares, Antonio
dc.contributor.authorVictor, Victor M.
dc.date.accessioned2026-02-10T12:13:56Z
dc.date.available2026-02-10T12:13:56Z
dc.date.issued2016
dc.identifier.citationDiaz-Morales, N., Rovira-Llopis, S., Bañuls, C., Escribano-Lopez, I., de Marañon, A. M., Lopez-Domenech, S., Orden, S., Roldan-Torres, I., Alvarez, A., Veses, S., Jover, A., Rocha, M., Hernandez-Mijares, A., & Victor, V. M. (2016). Are Mitochondrial Fusion and Fission Impaired in Leukocytes of Type 2 Diabetic Patients?. Antioxidants & redox signaling, 25(2), 108–115. https://doi.org/10.1089/ars.2016.6707es_ES
dc.identifier.issn1523-0864
dc.identifier.urihttp://hdl.handle.net/10366/169703
dc.description.abstract[EN]Mitochondrial fusion/fission alterations have been evaluated in different tissues of type 2 diabetic (T2D) patients. However, it is not known whether mitochondrial dynamics is disturbed in the leukocytes of T2D patients and whether glycemic control affects its regulation. Anthropometric and metabolic parameters in 91 T2D patients (48 with glycated hemoglobin [HbA1c] <6.5% and 43 with HbA1c >6.5%) were characteristic of the disease when compared with 78 control subjects. We observed increased reactive oxygen species production in leukocytes from diabetic patients, together with a reduced mitochondrial oxygen consumption rate, especially in poorly controlled patients. Mitochondrial fusion was reduced and fission was increased in diabetic patients, and both features were accentuated in patients with poor glycemic control. Furthermore, leukocyte rolling flux rose in parallel to HbA1c levels. The induction of leukocyte-endothelial interactions in diabetic patients was related to reduced mitochondrial fusion and higher mitochondrial fission. Our findings suggest that mitochondrial dynamics could be influenced by glycemic control in leukocytes of diabetic patients, in which there is decreased mitochondrial fusion and elevated fission related to enhanced leukocyte-endothelial interactions. These findings lead to the hypothesis that poor glycemic control during T2D may alter mitochondrial dynamics and could eventually promote leukocyte-endothelial interactions and the onset of cardiovascular diseaseses_ES
dc.description.sponsorshipFondo Europeo de Desarrollo Regional (FEDER), Instituto de Salud Carlos III (ISCIII), Ministerio de Ciencia e Innovación, CIBERehd, Generalitat Valencianaes_ES
dc.format.mimetypeapplication/pdf
dc.language.isoenges_ES
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectDiabetes mellitus tipo 2es_ES
dc.subjectMitocondriaes_ES
dc.subjectDinámica mitocondrial (Fusión y Fisión)es_ES
dc.subjectLeucocitoses_ES
dc.subjectEstrés oxidativoes_ES
dc.subjectMorfología mitocondriales_ES
dc.subjectControl glucémicoes_ES
dc.subjectAdhesión leucocitariaes_ES
dc.subjectType 2 Diabeteses_ES
dc.subjectMitochondriaes_ES
dc.subjectMitochondrial dynamics (Fusion and Fission)es_ES
dc.subjectLeukocyteses_ES
dc.subjectOxidative stresses_ES
dc.subjectMitochondrial morphologyes_ES
dc.subjectGlycemic controles_ES
dc.subjectleukocyte-endothelial interactionses_ES
dc.subject.meshDiabetes Mellitus, Type 2 *
dc.subject.meshOxidative Stress *
dc.subject.meshMitochondria *
dc.subject.meshMitochondrial Dynamics *
dc.subject.meshLeukocytes *
dc.titleAre Mitochondrial Fusion and Fission Impaired in Leukocytes of Type 2 Diabetic Patients?es_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publishversionhttps://doi.org/10.1089/ars.2016.6707es_ES
dc.subject.unesco3209 Farmacologíaes_ES
dc.subject.unesco2410.10 Fisiología Humanaes_ES
dc.subject.unesco2302 Bioquímicaes_ES
dc.subject.unesco2411.04 Fisiología Endocrinaes_ES
dc.subject.unesco2407 Biología Celulares_ES
dc.identifier.doi10.1089/ars.2016.6707
dc.relation.projectIDPI12/1984es_ES
dc.relation.projectIDPI13/1025es_ES
dc.relation.projectIDPI13/0073es_ES
dc.relation.projectIDPI15/1424es_ES
dc.relation.projectIDCB06/04/0071es_ES
dc.relation.projectIDPROMETEOII2014/035es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/embargoedAccesses_ES
dc.identifier.pmid27043041
dc.identifier.essn1557-7716
dc.journal.titleAntioxidants & Redox Signalinges_ES
dc.volume.number25es_ES
dc.issue.number2es_ES
dc.page.initial108es_ES
dc.page.final115es_ES
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones_ES
dc.subject.decsdiabetes mellitus tipo II *
dc.subject.decsmitocondrias *
dc.subject.decsestrés oxidativo *
dc.subject.decsdinámica mitocondrial *
dc.subject.decsleucocitos *


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