Hiperalfalipoproteinemia: uma revisão de literatura
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Research, Society and Development |
Texto Completo: | https://rsdjournal.org/index.php/rsd/article/view/37461 |
Resumo: | Objective: To analyze and address the causes and alterations related to hyperalphalipoproteinemia, comparing the general patterns of the population. Methodology: An Integrative Literature Review was conducted, in which key words specified in the Pubmed and Science Direct databases were used: "hyperalphalipoprotenemia" OUR "hyperalphalipoprotein" OUR "HDLc". Results: Mutations in individuals with hyperalphalipoproteinemia, single nucleotide polymorphisms, deleterious genes, cetp gene, hepatic SR-BI, endothelial lipase (EL) gene, splicing defect, genes and proteins ANGPTL3 and ANGPTL8 can be highlighted. In addition, changes in surface fluidity and HDLc membrane constituents were noted, changes in the RCT process and in the ability to increase expression and to activate endothelial synthesis of nitric oxide (NO). Furthermore, changes caused by CETP deficiency cannot be related to a cardioprotective, antiatherogenic and anti-inflammatory effect, and even a U-shaped relationship between plasma HDLc and ischemic electrocardiographic changes, where CETP deficiency accumulates. Moreover, the presence of the P376L variant, intervenenegatively in the processing of SR-BI. Finally, individuals with higher HDLc levels exhibit cholesterol particles enriched by apolipoproteins, which cause changes to the anti-inflammatory action of HDL itself. Conclusion: Changes in the physiological functioning of HDLc, which cause hyperalphalipoproteinemia, are caused by several mutations that lead to changes in the membrane mechanism, CETP, SR-BI and inflammatory processes. More research is needed to conclude about the cardioprotective effect. |
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Hiperalfalipoproteinemia: uma revisão de literaturaHyperalphalipoproteinemia: a literature reviewHiperalfalipoproteinemia: una revisión de la literaturaHiperalfalipoproteínaHDLCETPSR-BI.HyperalphalipoproteinHDLCETPSR-BI.HiperalfalipoproteínaHDLCETPSR-BI. Objective: To analyze and address the causes and alterations related to hyperalphalipoproteinemia, comparing the general patterns of the population. Methodology: An Integrative Literature Review was conducted, in which key words specified in the Pubmed and Science Direct databases were used: "hyperalphalipoprotenemia" OUR "hyperalphalipoprotein" OUR "HDLc". Results: Mutations in individuals with hyperalphalipoproteinemia, single nucleotide polymorphisms, deleterious genes, cetp gene, hepatic SR-BI, endothelial lipase (EL) gene, splicing defect, genes and proteins ANGPTL3 and ANGPTL8 can be highlighted. In addition, changes in surface fluidity and HDLc membrane constituents were noted, changes in the RCT process and in the ability to increase expression and to activate endothelial synthesis of nitric oxide (NO). Furthermore, changes caused by CETP deficiency cannot be related to a cardioprotective, antiatherogenic and anti-inflammatory effect, and even a U-shaped relationship between plasma HDLc and ischemic electrocardiographic changes, where CETP deficiency accumulates. Moreover, the presence of the P376L variant, intervenenegatively in the processing of SR-BI. Finally, individuals with higher HDLc levels exhibit cholesterol particles enriched by apolipoproteins, which cause changes to the anti-inflammatory action of HDL itself. Conclusion: Changes in the physiological functioning of HDLc, which cause hyperalphalipoproteinemia, are caused by several mutations that lead to changes in the membrane mechanism, CETP, SR-BI and inflammatory processes. More research is needed to conclude about the cardioprotective effect.Objetivo: Analisar e abordar as causas e as alterações relacionadas à hiperalfalipoproteinemia, tendo como comparação os padrões gerais da população. Metodologia: Realizou-se uma Revisão de Literatura Integrativa, na qual utilizou palavras chaves especificadas nas bases de dados Pubmed e Science Direct: “hyperalphalipoprotenemia” OUR “hyperalphalipoprotein” OUR “HDLc”. Resultados: Pode-se destacar as mutações em indivíduos com hiperalfalipoproteinemia os polimorfismos de nucleotídeo único, genes deletérios, gene que expressa o CETP, deleção de SR-BI hepático, gene da lipase endotelial (EL), defeito de splicing, genes e proteínas ANGPTL3 e ANGPTL8. Além disso, foram notadas alterações na fluidez superficial e constituintes da membrana do HDLc, alteração no processo de RCT e na capacidade de aumentar a expressão e por ativar a síntese endotelial do óxido nítrico (NO). Ademais, as alterações causadas por deficiência na CETP não podem ser relacionadas a um efeito cardioprotetor, antiaterogênico e anti inflamatório, sendo até encontrada uma relação em forma de U entre o HDLc plasmático e as alterações eletrocardiográficas isquêmicas, onde a deficiência de CETP se acumula. Outrossim, presença da variante P376L, intervêm negativamente no processamento de SR-BI. Por fim, indivíduos que apresentam níveis mais elevados HDLc, exibem partículas de colesterol enriquecidas por apolipoproteínas, as quais acarretam alterações a ação anti-inflamatória do próprio HDL. Conclusão: Alterações no funcionamento fisiológico do HDLc, que provocam a hiperalfalipoproteinemia, são causadas por diversas mutações que levam a alterações no mecanismo de membrana, CETP, SR-BI e processos inflamatórios. Faz-se necessárias mais pesquisas para concluir a respeito do efeito cardioprotetor.Objetivo: Analizar y abordar las causas y alteraciones relacionadas con la hiperalfalipoproteinemia, comparando los patrones generales de la población. Metodología: Se realizó una Revisión Integrativa de la Literatura, utilizando palabras clave especificadas en las bases de datos Pubmed y Science Direct: “hyperalphalipoprotenemia” OUR “hyperalphalipoprotein” OUR “HDLc”. Resultados: Se destacan mutaciones en individuos con hiperalfalipoproteinemia: polimorfismos de un solo nucleótido, genes deletéreos, gen que expresa CETP, deleción hepática SR-BI, gen de la lipasa endotelial (EL), defecto de splicing, genes y proteínas ANGPTL3 y ANGPTL8. Además, se observaron alteraciones en la fluidez superficial y constituyentes de membrana de HDLc, alteración en el proceso RCT y en la capacidad de aumentar la expresión y activar la síntesis endotelial de óxido nítrico (NO). Además, los cambios provocados por el déficit de CETP no pueden relacionarse con un efecto cardioprotector, antiaterogénico y antiinflamatorio, e incluso se ha encontrado una relación en forma de U entre el cHDL plasmático y los cambios electrocardiográficos isquémicos, donde se acumula el déficit de CETP. Además, la presencia de la variante P376L interfiere negativamente en el procesamiento de SR-BI. Finalmente, los individuos con niveles más altos de HDLc presentan partículas de colesterol enriquecidas en apolipoproteínas, que alteran la acción antiinflamatoria de las propias HDL. Conclusión: Los cambios en el funcionamiento fisiológico de HDLc, que causan hiperalfalipoproteinemia, son causados por varias mutaciones que conducen a cambios en el mecanismo de membrana, CETP, SR-BI y procesos inflamatorios. Se necesita más investigación para concluir sobre el efecto cardioprotector.Research, Society and Development2022-11-25info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://rsdjournal.org/index.php/rsd/article/view/3746110.33448/rsd-v11i15.37461Research, Society and Development; Vol. 11 No. 15; e525111537461Research, Society and Development; Vol. 11 Núm. 15; e525111537461Research, Society and Development; v. 11 n. 15; e5251115374612525-3409reponame:Research, Society and Developmentinstname:Universidade Federal de Itajubá (UNIFEI)instacron:UNIFEIporhttps://rsdjournal.org/index.php/rsd/article/view/37461/31256Copyright (c) 2022 Paula Rayssa Rodrigues; Lucas Martins; Alessandra Cristina Pupin Silvériohttps://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessRodrigues, Paula Rayssa Martins, Lucas Silvério, Alessandra Cristina Pupin2022-11-27T19:56:23Zoai:ojs.pkp.sfu.ca:article/37461Revistahttps://rsdjournal.org/index.php/rsd/indexPUBhttps://rsdjournal.org/index.php/rsd/oairsd.articles@gmail.com2525-34092525-3409opendoar:2024-01-17T09:51:37.544204Research, Society and Development - Universidade Federal de Itajubá (UNIFEI)false |
dc.title.none.fl_str_mv |
Hiperalfalipoproteinemia: uma revisão de literatura Hyperalphalipoproteinemia: a literature review Hiperalfalipoproteinemia: una revisión de la literatura |
title |
Hiperalfalipoproteinemia: uma revisão de literatura |
spellingShingle |
Hiperalfalipoproteinemia: uma revisão de literatura Rodrigues, Paula Rayssa Hiperalfalipoproteína HDL CETP SR-BI. Hyperalphalipoprotein HDL CETP SR-BI. Hiperalfalipoproteína HDL CETP SR-BI. |
title_short |
Hiperalfalipoproteinemia: uma revisão de literatura |
title_full |
Hiperalfalipoproteinemia: uma revisão de literatura |
title_fullStr |
Hiperalfalipoproteinemia: uma revisão de literatura |
title_full_unstemmed |
Hiperalfalipoproteinemia: uma revisão de literatura |
title_sort |
Hiperalfalipoproteinemia: uma revisão de literatura |
author |
Rodrigues, Paula Rayssa |
author_facet |
Rodrigues, Paula Rayssa Martins, Lucas Silvério, Alessandra Cristina Pupin |
author_role |
author |
author2 |
Martins, Lucas Silvério, Alessandra Cristina Pupin |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Rodrigues, Paula Rayssa Martins, Lucas Silvério, Alessandra Cristina Pupin |
dc.subject.por.fl_str_mv |
Hiperalfalipoproteína HDL CETP SR-BI. Hyperalphalipoprotein HDL CETP SR-BI. Hiperalfalipoproteína HDL CETP SR-BI. |
topic |
Hiperalfalipoproteína HDL CETP SR-BI. Hyperalphalipoprotein HDL CETP SR-BI. Hiperalfalipoproteína HDL CETP SR-BI. |
description |
Objective: To analyze and address the causes and alterations related to hyperalphalipoproteinemia, comparing the general patterns of the population. Methodology: An Integrative Literature Review was conducted, in which key words specified in the Pubmed and Science Direct databases were used: "hyperalphalipoprotenemia" OUR "hyperalphalipoprotein" OUR "HDLc". Results: Mutations in individuals with hyperalphalipoproteinemia, single nucleotide polymorphisms, deleterious genes, cetp gene, hepatic SR-BI, endothelial lipase (EL) gene, splicing defect, genes and proteins ANGPTL3 and ANGPTL8 can be highlighted. In addition, changes in surface fluidity and HDLc membrane constituents were noted, changes in the RCT process and in the ability to increase expression and to activate endothelial synthesis of nitric oxide (NO). Furthermore, changes caused by CETP deficiency cannot be related to a cardioprotective, antiatherogenic and anti-inflammatory effect, and even a U-shaped relationship between plasma HDLc and ischemic electrocardiographic changes, where CETP deficiency accumulates. Moreover, the presence of the P376L variant, intervenenegatively in the processing of SR-BI. Finally, individuals with higher HDLc levels exhibit cholesterol particles enriched by apolipoproteins, which cause changes to the anti-inflammatory action of HDL itself. Conclusion: Changes in the physiological functioning of HDLc, which cause hyperalphalipoproteinemia, are caused by several mutations that lead to changes in the membrane mechanism, CETP, SR-BI and inflammatory processes. More research is needed to conclude about the cardioprotective effect. |
publishDate |
2022 |
dc.date.none.fl_str_mv |
2022-11-25 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://rsdjournal.org/index.php/rsd/article/view/37461 10.33448/rsd-v11i15.37461 |
url |
https://rsdjournal.org/index.php/rsd/article/view/37461 |
identifier_str_mv |
10.33448/rsd-v11i15.37461 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.none.fl_str_mv |
https://rsdjournal.org/index.php/rsd/article/view/37461/31256 |
dc.rights.driver.fl_str_mv |
Copyright (c) 2022 Paula Rayssa Rodrigues; Lucas Martins; Alessandra Cristina Pupin Silvério https://creativecommons.org/licenses/by/4.0 info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
Copyright (c) 2022 Paula Rayssa Rodrigues; Lucas Martins; Alessandra Cristina Pupin Silvério 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 |
Research, Society and Development |
publisher.none.fl_str_mv |
Research, Society and Development |
dc.source.none.fl_str_mv |
Research, Society and Development; Vol. 11 No. 15; e525111537461 Research, Society and Development; Vol. 11 Núm. 15; e525111537461 Research, Society and Development; v. 11 n. 15; e525111537461 2525-3409 reponame:Research, Society and Development instname:Universidade Federal de Itajubá (UNIFEI) instacron:UNIFEI |
instname_str |
Universidade Federal de Itajubá (UNIFEI) |
instacron_str |
UNIFEI |
institution |
UNIFEI |
reponame_str |
Research, Society and Development |
collection |
Research, Society and Development |
repository.name.fl_str_mv |
Research, Society and Development - Universidade Federal de Itajubá (UNIFEI) |
repository.mail.fl_str_mv |
rsd.articles@gmail.com |
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1797052828030599168 |