Endothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetes

Detalhes bibliográficos
Autor(a) principal: Boff, Winston
Data de Publicação: 2015
Outros Autores: Wainstein, Marco Vugman, Puñales, Márcia Khaled, Silva, Antônio Marcos Vargas da, Cé, Gislaine Vissoky, Bertoluci, Marcello Casaccia
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UFRGS
Texto Completo: http://hdl.handle.net/10183/196841
Resumo: Macro and microvascular disease are the main cause of morbi-mortality in type 1 diabetes (T1DM). Although there is a clear association between endothelial dysfunction and atherosclerosis in type 2 diabetes, a cause-effect relationship is less clear in T1DM. Although endothelial dysfunction (ED) precedes atherosclerosis, it is not clear weather, in recent onset T1DM, it may progress to clinical macrovascular disease. Moreover, endothelial dysfunction may either be reversed spontaneously or in response to intensive glycemic control, long-term exercise training and use of statins. Acute, long-term and post-prandial hyperglycemia as well as duration of diabetes and microalbuminuria are all conditions associated with ED in T1DM. The pathogenesis of endothelial dysfunction is closely related to oxidative-stress. NAD(P)H oxidase over activity induces excessive superoxide production inside the mitochondrial oxidative chain of endothelial cells, thus reducing nitric oxide bioavailability and resulting in peroxynitrite formation, a potent oxidant agent. Moreover, oxidative stress also uncouples endothelial nitric oxide synthase, which becomes dysfunctional, inducing formation of superoxide. Other important mechanisms are the activation of both the polyol and protein kinase C pathways as well as the presence of advanced glycation end-products. Future studies are needed to evaluate the potential clinical applicability of endothelial dysfunction as a marker for early vascular complications in T1DM.
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spelling Boff, WinstonWainstein, Marco VugmanPuñales, Márcia KhaledSilva, Antônio Marcos Vargas daCé, Gislaine VissokyBertoluci, Marcello Casaccia2019-07-12T02:36:09Z20151948-9358http://hdl.handle.net/10183/196841000989727Macro and microvascular disease are the main cause of morbi-mortality in type 1 diabetes (T1DM). Although there is a clear association between endothelial dysfunction and atherosclerosis in type 2 diabetes, a cause-effect relationship is less clear in T1DM. Although endothelial dysfunction (ED) precedes atherosclerosis, it is not clear weather, in recent onset T1DM, it may progress to clinical macrovascular disease. Moreover, endothelial dysfunction may either be reversed spontaneously or in response to intensive glycemic control, long-term exercise training and use of statins. Acute, long-term and post-prandial hyperglycemia as well as duration of diabetes and microalbuminuria are all conditions associated with ED in T1DM. The pathogenesis of endothelial dysfunction is closely related to oxidative-stress. NAD(P)H oxidase over activity induces excessive superoxide production inside the mitochondrial oxidative chain of endothelial cells, thus reducing nitric oxide bioavailability and resulting in peroxynitrite formation, a potent oxidant agent. Moreover, oxidative stress also uncouples endothelial nitric oxide synthase, which becomes dysfunctional, inducing formation of superoxide. Other important mechanisms are the activation of both the polyol and protein kinase C pathways as well as the presence of advanced glycation end-products. Future studies are needed to evaluate the potential clinical applicability of endothelial dysfunction as a marker for early vascular complications in T1DM.application/pdfengWorld Journal of Diabetes. Pleasanton, CA. Vol. 6, n. 5 (Jun. 2015), p. 679-692Diabetes mellitus tipo 1Doenças cardiovascularesEndothelial dysfunctionType 1 diabetesCardiovascular diseaseEndothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetesinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/otherinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT000989727.pdf.txt000989727.pdf.txtExtracted Texttext/plain81023http://www.lume.ufrgs.br/bitstream/10183/196841/2/000989727.pdf.txtdc05c520d390c8aadaff8d3e1781dcb8MD52ORIGINAL000989727.pdfTexto completo (inglês)application/pdf1005118http://www.lume.ufrgs.br/bitstream/10183/196841/1/000989727.pdfa1ded153b1bae564f6336ce988b64c80MD5110183/1968412019-07-13 02:35:55.417678oai:www.lume.ufrgs.br:10183/196841Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2019-07-13T05:35:55Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false
dc.title.pt_BR.fl_str_mv Endothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetes
title Endothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetes
spellingShingle Endothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetes
Boff, Winston
Diabetes mellitus tipo 1
Doenças cardiovasculares
Endothelial dysfunction
Type 1 diabetes
Cardiovascular disease
title_short Endothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetes
title_full Endothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetes
title_fullStr Endothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetes
title_full_unstemmed Endothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetes
title_sort Endothelial dysfunction as a predictor of cardiovascular disease in type 1 diabetes
author Boff, Winston
author_facet Boff, Winston
Wainstein, Marco Vugman
Puñales, Márcia Khaled
Silva, Antônio Marcos Vargas da
Cé, Gislaine Vissoky
Bertoluci, Marcello Casaccia
author_role author
author2 Wainstein, Marco Vugman
Puñales, Márcia Khaled
Silva, Antônio Marcos Vargas da
Cé, Gislaine Vissoky
Bertoluci, Marcello Casaccia
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Boff, Winston
Wainstein, Marco Vugman
Puñales, Márcia Khaled
Silva, Antônio Marcos Vargas da
Cé, Gislaine Vissoky
Bertoluci, Marcello Casaccia
dc.subject.por.fl_str_mv Diabetes mellitus tipo 1
Doenças cardiovasculares
topic Diabetes mellitus tipo 1
Doenças cardiovasculares
Endothelial dysfunction
Type 1 diabetes
Cardiovascular disease
dc.subject.eng.fl_str_mv Endothelial dysfunction
Type 1 diabetes
Cardiovascular disease
description Macro and microvascular disease are the main cause of morbi-mortality in type 1 diabetes (T1DM). Although there is a clear association between endothelial dysfunction and atherosclerosis in type 2 diabetes, a cause-effect relationship is less clear in T1DM. Although endothelial dysfunction (ED) precedes atherosclerosis, it is not clear weather, in recent onset T1DM, it may progress to clinical macrovascular disease. Moreover, endothelial dysfunction may either be reversed spontaneously or in response to intensive glycemic control, long-term exercise training and use of statins. Acute, long-term and post-prandial hyperglycemia as well as duration of diabetes and microalbuminuria are all conditions associated with ED in T1DM. The pathogenesis of endothelial dysfunction is closely related to oxidative-stress. NAD(P)H oxidase over activity induces excessive superoxide production inside the mitochondrial oxidative chain of endothelial cells, thus reducing nitric oxide bioavailability and resulting in peroxynitrite formation, a potent oxidant agent. Moreover, oxidative stress also uncouples endothelial nitric oxide synthase, which becomes dysfunctional, inducing formation of superoxide. Other important mechanisms are the activation of both the polyol and protein kinase C pathways as well as the presence of advanced glycation end-products. Future studies are needed to evaluate the potential clinical applicability of endothelial dysfunction as a marker for early vascular complications in T1DM.
publishDate 2015
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dc.relation.ispartof.pt_BR.fl_str_mv World Journal of Diabetes. Pleasanton, CA. Vol. 6, n. 5 (Jun. 2015), p. 679-692
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