Melatonina: modulador de morte celular
Autor(a) principal: | |
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Data de Publicação: | 2010 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://dx.doi.org/10.1590/S0104-42302010000600024 http://repositorio.unifesp.br/handle/11600/5489 |
Resumo: | Apoptosis or programmed death is a biological phenomenon, which is essential for the development and maintenance of a cell population. In this process, senescent or damaged cells are eliminated after activation of a cell death program involving participation of pro-apoptotic molecules (Fas, Fas-L, Bax, caspases 2, 3, 6, 7, 8 and 9). Molecule activation causes typical morphological changes, such as cell shrinkage, loss of adhesion to the extracellular matrix and neighboring cells, chromatin condensation, DNA fragmentation and formation of apoptotic bodies. Anti-apoptotic molecules (Bcl-2, FLIP) block the emergence and evolution of these cell changes and prevent cell death. The balance between molecules pro and anti-apoptotic ensures tissue homeostasis. When apoptosis is out of control, it contributes to the emergence of several neoplastic, autoimmune and neurodegenerative diseases. Several inducing and inhibitors of apoptosis agents are recognized as potential weapons in the fight against diseases related to proliferation and cell death disorders among which stand out hormones. Melatonin has been reported as important anti-apoptotic agent in various tissues by reducing cell calcium uptake, modulating expression of anti-oxidants and decreasing pro-apoptotic protein, such as Bax. The knowledge of new agents capable to act on the course pf apoptosis is important and of great value for developing further therapies against many diseases. Thus, the objective of this review was to elucidate the main aspects of cell death by apoptosis and the role of melatonin in this process. |
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Melatonina: modulador de morte celularMelatonin: cell death modulatorMelatoninPineal glandApoptosisApoptosis regulatory proteinsCaspasesMelatoninaGlândula pinealApoptoseCaspasesProteínas reguladoras de apoptoseApoptosis or programmed death is a biological phenomenon, which is essential for the development and maintenance of a cell population. In this process, senescent or damaged cells are eliminated after activation of a cell death program involving participation of pro-apoptotic molecules (Fas, Fas-L, Bax, caspases 2, 3, 6, 7, 8 and 9). Molecule activation causes typical morphological changes, such as cell shrinkage, loss of adhesion to the extracellular matrix and neighboring cells, chromatin condensation, DNA fragmentation and formation of apoptotic bodies. Anti-apoptotic molecules (Bcl-2, FLIP) block the emergence and evolution of these cell changes and prevent cell death. The balance between molecules pro and anti-apoptotic ensures tissue homeostasis. When apoptosis is out of control, it contributes to the emergence of several neoplastic, autoimmune and neurodegenerative diseases. Several inducing and inhibitors of apoptosis agents are recognized as potential weapons in the fight against diseases related to proliferation and cell death disorders among which stand out hormones. Melatonin has been reported as important anti-apoptotic agent in various tissues by reducing cell calcium uptake, modulating expression of anti-oxidants and decreasing pro-apoptotic protein, such as Bax. The knowledge of new agents capable to act on the course pf apoptosis is important and of great value for developing further therapies against many diseases. Thus, the objective of this review was to elucidate the main aspects of cell death by apoptosis and the role of melatonin in this process.A apoptose ou morte programada é um fenômeno biológico essencial para o desenvolvimento e manutenção de uma população celular. Neste processo, as células senescentes ou indesejáveis são eliminadas após ativação de um programa de morte celular, que envolve a participação de moléculas pró-apoptóticas (Fas, FasL, Bax, Caspases 2, 3, 6, 7, 8 e 9). A ativação destas moléculas provoca típicas alterações morfológicas como a retração celular, perda de aderência à matriz extracelular e às células vizinhas, condensação da cromatina, fragmentação do DNA e formação de corpos apoptóticos. Moléculas antiapoptóticas (Bcl2, FLIP) bloqueiam o surgimento e a evolução destas alterações celulares e evitam a morte celular. É o equilíbrio entre moléculas pró e antiapoptóticas que assegura a homeostase tecidual. O descontrole da apoptose pode contribuir para o aparecimento de diversas doenças neoplásicas, autoimunes e neurodegenerativas. Diversos agentes indutores e inibidores de apoptose são reconhecidos como armas potenciais no combate a doenças relacionadas a distúrbios de proliferação e morte celular, dentre eles, destacam-se os hormônios. A melatonina tem sido relatada com importante ação antiápoptótica em diversos tecidos, modulando a expressão de agentes, reduzindo a entrada de cálcio na célula, bem como atenuando a produção de espécies reativas de oxigênio e de proteínas pró-apoptóticas, tal como, diminuição da Bax. O conhecimento de novos agentes capazes de atuar nas vias da apoptose é de grande valia para o desenvolvimento de futuras terapias no tratamento de diversas doenças. Assim, o objetivo dessa revisão é elucidar os principais aspectos da morte celular pela apoptose e o papel da melatonina neste processo.Universidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Departamento de GinecologiaUniversidade de São Paulo Faculdade de Medicina Departamento de Obstetrícia e GinecologiaUNIFESP, EPM, Depto. de GinecologiaSciELOAssociação Médica BrasileiraUniversidade Federal de São Paulo (UNIFESP)Universidade de São Paulo (USP)Ferreira, Cecília da Silva [UNIFESP]Maganhin, Carla Cristina [UNIFESP]Simões, Ricardo dos SantosGirão, Manoel João Batista Castello [UNIFESP]Baracat, Edmund Chada [UNIFESP]Soares Junior, José Maria [UNIFESP]2015-06-14T13:41:24Z2015-06-14T13:41:24Z2010-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion715-718application/pdfhttp://dx.doi.org/10.1590/S0104-42302010000600024Revista da Associação Médica Brasileira. Associação Médica Brasileira, v. 56, n. 6, p. 715-718, 2010.10.1590/S0104-42302010000600024S0104-42302010000600024.pdf0104-4230S0104-42302010000600024http://repositorio.unifesp.br/handle/11600/5489WOS:000286619200023porRevista da Associação Médica Brasileirainfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-07-29T22:37:59Zoai:repositorio.unifesp.br/:11600/5489Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-07-29T22:37:59Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
Melatonina: modulador de morte celular Melatonin: cell death modulator |
title |
Melatonina: modulador de morte celular |
spellingShingle |
Melatonina: modulador de morte celular Ferreira, Cecília da Silva [UNIFESP] Melatonin Pineal gland Apoptosis Apoptosis regulatory proteins Caspases Melatonina Glândula pineal Apoptose Caspases Proteínas reguladoras de apoptose |
title_short |
Melatonina: modulador de morte celular |
title_full |
Melatonina: modulador de morte celular |
title_fullStr |
Melatonina: modulador de morte celular |
title_full_unstemmed |
Melatonina: modulador de morte celular |
title_sort |
Melatonina: modulador de morte celular |
author |
Ferreira, Cecília da Silva [UNIFESP] |
author_facet |
Ferreira, Cecília da Silva [UNIFESP] Maganhin, Carla Cristina [UNIFESP] Simões, Ricardo dos Santos Girão, Manoel João Batista Castello [UNIFESP] Baracat, Edmund Chada [UNIFESP] Soares Junior, José Maria [UNIFESP] |
author_role |
author |
author2 |
Maganhin, Carla Cristina [UNIFESP] Simões, Ricardo dos Santos Girão, Manoel João Batista Castello [UNIFESP] Baracat, Edmund Chada [UNIFESP] Soares Junior, José Maria [UNIFESP] |
author2_role |
author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) Universidade de São Paulo (USP) |
dc.contributor.author.fl_str_mv |
Ferreira, Cecília da Silva [UNIFESP] Maganhin, Carla Cristina [UNIFESP] Simões, Ricardo dos Santos Girão, Manoel João Batista Castello [UNIFESP] Baracat, Edmund Chada [UNIFESP] Soares Junior, José Maria [UNIFESP] |
dc.subject.por.fl_str_mv |
Melatonin Pineal gland Apoptosis Apoptosis regulatory proteins Caspases Melatonina Glândula pineal Apoptose Caspases Proteínas reguladoras de apoptose |
topic |
Melatonin Pineal gland Apoptosis Apoptosis regulatory proteins Caspases Melatonina Glândula pineal Apoptose Caspases Proteínas reguladoras de apoptose |
description |
Apoptosis or programmed death is a biological phenomenon, which is essential for the development and maintenance of a cell population. In this process, senescent or damaged cells are eliminated after activation of a cell death program involving participation of pro-apoptotic molecules (Fas, Fas-L, Bax, caspases 2, 3, 6, 7, 8 and 9). Molecule activation causes typical morphological changes, such as cell shrinkage, loss of adhesion to the extracellular matrix and neighboring cells, chromatin condensation, DNA fragmentation and formation of apoptotic bodies. Anti-apoptotic molecules (Bcl-2, FLIP) block the emergence and evolution of these cell changes and prevent cell death. The balance between molecules pro and anti-apoptotic ensures tissue homeostasis. When apoptosis is out of control, it contributes to the emergence of several neoplastic, autoimmune and neurodegenerative diseases. Several inducing and inhibitors of apoptosis agents are recognized as potential weapons in the fight against diseases related to proliferation and cell death disorders among which stand out hormones. Melatonin has been reported as important anti-apoptotic agent in various tissues by reducing cell calcium uptake, modulating expression of anti-oxidants and decreasing pro-apoptotic protein, such as Bax. The knowledge of new agents capable to act on the course pf apoptosis is important and of great value for developing further therapies against many diseases. Thus, the objective of this review was to elucidate the main aspects of cell death by apoptosis and the role of melatonin in this process. |
publishDate |
2010 |
dc.date.none.fl_str_mv |
2010-01-01 2015-06-14T13:41:24Z 2015-06-14T13:41:24Z |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1590/S0104-42302010000600024 Revista da Associação Médica Brasileira. Associação Médica Brasileira, v. 56, n. 6, p. 715-718, 2010. 10.1590/S0104-42302010000600024 S0104-42302010000600024.pdf 0104-4230 S0104-42302010000600024 http://repositorio.unifesp.br/handle/11600/5489 WOS:000286619200023 |
url |
http://dx.doi.org/10.1590/S0104-42302010000600024 http://repositorio.unifesp.br/handle/11600/5489 |
identifier_str_mv |
Revista da Associação Médica Brasileira. Associação Médica Brasileira, v. 56, n. 6, p. 715-718, 2010. 10.1590/S0104-42302010000600024 S0104-42302010000600024.pdf 0104-4230 S0104-42302010000600024 WOS:000286619200023 |
dc.language.iso.fl_str_mv |
por |
language |
por |
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Revista da Associação Médica Brasileira |
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info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
715-718 application/pdf |
dc.publisher.none.fl_str_mv |
Associação Médica Brasileira |
publisher.none.fl_str_mv |
Associação Médica Brasileira |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
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Universidade Federal de São Paulo (UNIFESP) |
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UNIFESP |
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UNIFESP |
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Repositório Institucional da UNIFESP |
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Repositório Institucional da UNIFESP |
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Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
biblioteca.csp@unifesp.br |
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1814268428462063616 |