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Necroptosis: a regulated inflammatory mode of cell death
Programmed cell death has a vital role in embryonic development and tissue homeostasis. Necroptosis is an alternative mode of regulated cell death mimicking features of apoptosis and necrosis. Necroptosis requires protein RIPK3 (previously well recognized as regulator of inflammation, cell survival,...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6035417/ https://www.ncbi.nlm.nih.gov/pubmed/29980212 http://dx.doi.org/10.1186/s12974-018-1235-0 |
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author | Dhuriya, Yogesh K. Sharma, Divakar |
author_facet | Dhuriya, Yogesh K. Sharma, Divakar |
author_sort | Dhuriya, Yogesh K. |
collection | PubMed |
description | Programmed cell death has a vital role in embryonic development and tissue homeostasis. Necroptosis is an alternative mode of regulated cell death mimicking features of apoptosis and necrosis. Necroptosis requires protein RIPK3 (previously well recognized as regulator of inflammation, cell survival, and disease) and its substrate MLKL, the crucial players of this pathway. Necroptosis is induced by toll-like receptor, death receptor, interferon, and some other mediators. Shreds of evidence based on a mouse model reveals that deregulation of necroptosis has been found to be associated with pathological conditions like cancer, neurodegenerative diseases, and inflammatory diseases. In this timeline article, we are discussing the molecular mechanisms of necroptosis and its relevance to diseases. |
format | Online Article Text |
id | pubmed-6035417 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-60354172018-07-09 Necroptosis: a regulated inflammatory mode of cell death Dhuriya, Yogesh K. Sharma, Divakar J Neuroinflammation Review Programmed cell death has a vital role in embryonic development and tissue homeostasis. Necroptosis is an alternative mode of regulated cell death mimicking features of apoptosis and necrosis. Necroptosis requires protein RIPK3 (previously well recognized as regulator of inflammation, cell survival, and disease) and its substrate MLKL, the crucial players of this pathway. Necroptosis is induced by toll-like receptor, death receptor, interferon, and some other mediators. Shreds of evidence based on a mouse model reveals that deregulation of necroptosis has been found to be associated with pathological conditions like cancer, neurodegenerative diseases, and inflammatory diseases. In this timeline article, we are discussing the molecular mechanisms of necroptosis and its relevance to diseases. BioMed Central 2018-07-06 /pmc/articles/PMC6035417/ /pubmed/29980212 http://dx.doi.org/10.1186/s12974-018-1235-0 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Review Dhuriya, Yogesh K. Sharma, Divakar Necroptosis: a regulated inflammatory mode of cell death |
title | Necroptosis: a regulated inflammatory mode of cell death |
title_full | Necroptosis: a regulated inflammatory mode of cell death |
title_fullStr | Necroptosis: a regulated inflammatory mode of cell death |
title_full_unstemmed | Necroptosis: a regulated inflammatory mode of cell death |
title_short | Necroptosis: a regulated inflammatory mode of cell death |
title_sort | necroptosis: a regulated inflammatory mode of cell death |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6035417/ https://www.ncbi.nlm.nih.gov/pubmed/29980212 http://dx.doi.org/10.1186/s12974-018-1235-0 |
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