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Necroptosis, necrostatins and tissue injury

Cell death is an integral part of the life of an organism being necessary for the maintenance of organs and tissues. If, however, cell death is allowed to proceed unrestricted, tissue damage and degenerative disease may ensue. Until recently, three morphologically distinct types of cell death were r...

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Detalles Bibliográficos
Autores principales: Smith, Christopher CT, Yellon, Derek M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918037/
https://www.ncbi.nlm.nih.gov/pubmed/21564515
http://dx.doi.org/10.1111/j.1582-4934.2011.01341.x
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author Smith, Christopher CT
Yellon, Derek M
author_facet Smith, Christopher CT
Yellon, Derek M
author_sort Smith, Christopher CT
collection PubMed
description Cell death is an integral part of the life of an organism being necessary for the maintenance of organs and tissues. If, however, cell death is allowed to proceed unrestricted, tissue damage and degenerative disease may ensue. Until recently, three morphologically distinct types of cell death were recognized, apoptosis (type I), autophagy (type II) and necrosis (type III). Apoptosis is a highly regulated, genetically determined mechanism designed to dismantle cells systematically (e.g. cells that are no longer functionally viable), via protease (caspase) action, and maintain homeostasis. Autophagy is responsible for the degradation of cytoplasmic material, e.g. proteins and organelles, through autophagosome formation and subsequent proteolytic degradation by lysosomes, and is normally considered in the context of survival although it is sometimes associated with cell death. Necrosis was formerly considered to be an accidental, unregulated form of cell death resulting from excessive stress, although it has been suggested that this is an over-simplistic view as necrosis may under certain circumstances involve the mobilization of specific transduction mechanisms. Indeed, recently, an alternative death pathway, termed necroptosis, was delineated and proposed as a form of ‘programmed necrosis’. Identified with the aid of specific inhibitors called necrostatins, necroptosis shares characteristics with both necrosis and apoptosis. Necroptosis involves Fas/tumour necrosis factor-α death domain receptor activation and inhibition of receptor-interacting protein I kinase, and it has been suggested that it may contribute to the development of neurological and myocardial diseases. Significantly, necrostatin-like drugs have been mooted as possible future therapeutic agents for the treatment of degenerative conditions.
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spelling pubmed-39180372015-04-06 Necroptosis, necrostatins and tissue injury Smith, Christopher CT Yellon, Derek M J Cell Mol Med Reviews Cell death is an integral part of the life of an organism being necessary for the maintenance of organs and tissues. If, however, cell death is allowed to proceed unrestricted, tissue damage and degenerative disease may ensue. Until recently, three morphologically distinct types of cell death were recognized, apoptosis (type I), autophagy (type II) and necrosis (type III). Apoptosis is a highly regulated, genetically determined mechanism designed to dismantle cells systematically (e.g. cells that are no longer functionally viable), via protease (caspase) action, and maintain homeostasis. Autophagy is responsible for the degradation of cytoplasmic material, e.g. proteins and organelles, through autophagosome formation and subsequent proteolytic degradation by lysosomes, and is normally considered in the context of survival although it is sometimes associated with cell death. Necrosis was formerly considered to be an accidental, unregulated form of cell death resulting from excessive stress, although it has been suggested that this is an over-simplistic view as necrosis may under certain circumstances involve the mobilization of specific transduction mechanisms. Indeed, recently, an alternative death pathway, termed necroptosis, was delineated and proposed as a form of ‘programmed necrosis’. Identified with the aid of specific inhibitors called necrostatins, necroptosis shares characteristics with both necrosis and apoptosis. Necroptosis involves Fas/tumour necrosis factor-α death domain receptor activation and inhibition of receptor-interacting protein I kinase, and it has been suggested that it may contribute to the development of neurological and myocardial diseases. Significantly, necrostatin-like drugs have been mooted as possible future therapeutic agents for the treatment of degenerative conditions. Blackwell Publishing Ltd 2011-09 2011-08-28 /pmc/articles/PMC3918037/ /pubmed/21564515 http://dx.doi.org/10.1111/j.1582-4934.2011.01341.x Text en © 2011 The Authors Journal compilation © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd
spellingShingle Reviews
Smith, Christopher CT
Yellon, Derek M
Necroptosis, necrostatins and tissue injury
title Necroptosis, necrostatins and tissue injury
title_full Necroptosis, necrostatins and tissue injury
title_fullStr Necroptosis, necrostatins and tissue injury
title_full_unstemmed Necroptosis, necrostatins and tissue injury
title_short Necroptosis, necrostatins and tissue injury
title_sort necroptosis, necrostatins and tissue injury
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3918037/
https://www.ncbi.nlm.nih.gov/pubmed/21564515
http://dx.doi.org/10.1111/j.1582-4934.2011.01341.x
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