Myocardial Insulin Resistance
Autor(a) principal: | |
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Data de Publicação: | 2021 |
Outros Autores: | , , |
Tipo de documento: | preprint |
Idioma: | eng |
Título da fonte: | SciELO Preprints |
Texto Completo: | https://preprints.scielo.org/index.php/scielo/preprint/view/3332 |
Resumo: | Background: The low available of Glut-4 transporters in sarcolemma of the cardiac cells is what characterizes the myocardial insulin resistance (MIR), which is triggered separately of generalized insulin resistance. Insulin receptors are quite evident in the heart muscle and vessels, and mitochondrial activity performs a significant function in MIR preserving cellular homeostasis by cell reproduction, cells livelihoods, and energy generation. Objective: To evaluate the MIR mechanism and through the signaling pathway design. Methods: PubMed database was employed to search for reviews publications with MIR. The referenced data of the signaling pathway was chosen aggregating references of the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. A signaling pathway was designed based on MIR research manuscripts, where we show several mechanisms included in the MIR. The KEGG server was employed to exploit the interrelationship protein-protein, and elaborate signaling pathway diagram. The signaling pathway mapping was carried out with PathVisio software. Results: We selected 42 articles from a total of 450 articles in the PubMed database that presented a significant association between the terms "insulin resistance myocardial" AND "signaling pathway". Founded on database-validated research papers, we choose well-founded pathways and we succeeded representative description of these pathways. The reproduction contigs taken from the KEGG database designed the signaling pathway of the bio-molecules that lead to MIR. Thus, the acting among multiple mechanisms releases factors that participate of the development of MIR. Conclusion: The interaction among various mechanisms and molecular interactions are important factors in development of MIR. |
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Myocardial Insulin ResistanceMyocardialInsulin resistanceSignaling pathwayBackground: The low available of Glut-4 transporters in sarcolemma of the cardiac cells is what characterizes the myocardial insulin resistance (MIR), which is triggered separately of generalized insulin resistance. Insulin receptors are quite evident in the heart muscle and vessels, and mitochondrial activity performs a significant function in MIR preserving cellular homeostasis by cell reproduction, cells livelihoods, and energy generation. Objective: To evaluate the MIR mechanism and through the signaling pathway design. Methods: PubMed database was employed to search for reviews publications with MIR. The referenced data of the signaling pathway was chosen aggregating references of the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. A signaling pathway was designed based on MIR research manuscripts, where we show several mechanisms included in the MIR. The KEGG server was employed to exploit the interrelationship protein-protein, and elaborate signaling pathway diagram. The signaling pathway mapping was carried out with PathVisio software. Results: We selected 42 articles from a total of 450 articles in the PubMed database that presented a significant association between the terms "insulin resistance myocardial" AND "signaling pathway". Founded on database-validated research papers, we choose well-founded pathways and we succeeded representative description of these pathways. The reproduction contigs taken from the KEGG database designed the signaling pathway of the bio-molecules that lead to MIR. Thus, the acting among multiple mechanisms releases factors that participate of the development of MIR. Conclusion: The interaction among various mechanisms and molecular interactions are important factors in development of MIR.SciELO PreprintsSciELO PreprintsSciELO Preprints2021-12-08info:eu-repo/semantics/preprintinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://preprints.scielo.org/index.php/scielo/preprint/view/333210.1590/SciELOPreprints.3332enghttps://preprints.scielo.org/index.php/scielo/article/view/3332/5986Copyright (c) 2021 Luis Jesuino de Oliveira Andrade, Ingrid Silva Santos Padilha, Luís Matos de Oliveira, Gabriela Correia Matos de Oliveirahttps://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessde Oliveira Andrade, Luis JesuinoSantos Padilha, Ingrid SilvaMatos de Oliveira, LuísMatos de Oliveira, Gabriela Correiareponame:SciELO Preprintsinstname:SciELOinstacron:SCI2021-12-07T23:22:10Zoai:ops.preprints.scielo.org:preprint/3332Servidor de preprintshttps://preprints.scielo.org/index.php/scieloONGhttps://preprints.scielo.org/index.php/scielo/oaiscielo.submission@scielo.orgopendoar:2021-12-07T23:22:10SciELO Preprints - SciELOfalse |
dc.title.none.fl_str_mv |
Myocardial Insulin Resistance |
title |
Myocardial Insulin Resistance |
spellingShingle |
Myocardial Insulin Resistance de Oliveira Andrade, Luis Jesuino Myocardial Insulin resistance Signaling pathway |
title_short |
Myocardial Insulin Resistance |
title_full |
Myocardial Insulin Resistance |
title_fullStr |
Myocardial Insulin Resistance |
title_full_unstemmed |
Myocardial Insulin Resistance |
title_sort |
Myocardial Insulin Resistance |
author |
de Oliveira Andrade, Luis Jesuino |
author_facet |
de Oliveira Andrade, Luis Jesuino Santos Padilha, Ingrid Silva Matos de Oliveira, Luís Matos de Oliveira, Gabriela Correia |
author_role |
author |
author2 |
Santos Padilha, Ingrid Silva Matos de Oliveira, Luís Matos de Oliveira, Gabriela Correia |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
de Oliveira Andrade, Luis Jesuino Santos Padilha, Ingrid Silva Matos de Oliveira, Luís Matos de Oliveira, Gabriela Correia |
dc.subject.por.fl_str_mv |
Myocardial Insulin resistance Signaling pathway |
topic |
Myocardial Insulin resistance Signaling pathway |
description |
Background: The low available of Glut-4 transporters in sarcolemma of the cardiac cells is what characterizes the myocardial insulin resistance (MIR), which is triggered separately of generalized insulin resistance. Insulin receptors are quite evident in the heart muscle and vessels, and mitochondrial activity performs a significant function in MIR preserving cellular homeostasis by cell reproduction, cells livelihoods, and energy generation. Objective: To evaluate the MIR mechanism and through the signaling pathway design. Methods: PubMed database was employed to search for reviews publications with MIR. The referenced data of the signaling pathway was chosen aggregating references of the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. A signaling pathway was designed based on MIR research manuscripts, where we show several mechanisms included in the MIR. The KEGG server was employed to exploit the interrelationship protein-protein, and elaborate signaling pathway diagram. The signaling pathway mapping was carried out with PathVisio software. Results: We selected 42 articles from a total of 450 articles in the PubMed database that presented a significant association between the terms "insulin resistance myocardial" AND "signaling pathway". Founded on database-validated research papers, we choose well-founded pathways and we succeeded representative description of these pathways. The reproduction contigs taken from the KEGG database designed the signaling pathway of the bio-molecules that lead to MIR. Thus, the acting among multiple mechanisms releases factors that participate of the development of MIR. Conclusion: The interaction among various mechanisms and molecular interactions are important factors in development of MIR. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-12-08 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/preprint info:eu-repo/semantics/publishedVersion |
format |
preprint |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://preprints.scielo.org/index.php/scielo/preprint/view/3332 10.1590/SciELOPreprints.3332 |
url |
https://preprints.scielo.org/index.php/scielo/preprint/view/3332 |
identifier_str_mv |
10.1590/SciELOPreprints.3332 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
https://preprints.scielo.org/index.php/scielo/article/view/3332/5986 |
dc.rights.driver.fl_str_mv |
https://creativecommons.org/licenses/by/4.0 info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/4.0 |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
SciELO Preprints SciELO Preprints SciELO Preprints |
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SciELO Preprints SciELO Preprints SciELO Preprints |
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SciELO |
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SciELO Preprints |
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SciELO Preprints |
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SciELO Preprints - SciELO |
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scielo.submission@scielo.org |
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1797047825880580096 |