Cargando…

Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications

Inflammasomes are high molecular weight protein complexes in the cytosol of immune and other cells that play a critical role in the innate immune system in response to cellular stress. NLRP3 inflammasome, the best-understood inflammasome, is known to mediate the maturation (activation) of caspase-1...

Descripción completa

Detalles Bibliográficos
Autores principales: Chen, Gong, Chelu, Mihail G., Dobrev, Dobromir, Li, Na
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6100656/
https://www.ncbi.nlm.nih.gov/pubmed/30150941
http://dx.doi.org/10.3389/fphys.2018.01115
_version_ 1783348924223848448
author Chen, Gong
Chelu, Mihail G.
Dobrev, Dobromir
Li, Na
author_facet Chen, Gong
Chelu, Mihail G.
Dobrev, Dobromir
Li, Na
author_sort Chen, Gong
collection PubMed
description Inflammasomes are high molecular weight protein complexes in the cytosol of immune and other cells that play a critical role in the innate immune system in response to cellular stress. NLRP3 inflammasome, the best-understood inflammasome, is known to mediate the maturation (activation) of caspase-1 from pro-caspase-1, causing the maturation and release of cytokines (e.g., interleukin-1β) and potentially leading to a form of inflammatory programmed cell death called pyroptosis. Previous work has shown that the NLRP3 components are expressed in cardiomyocytes and cardiac fibroblasts and recent studies have identified the NLRP3 inflammasome as a key nodal point in the pathogenesis of cardiomyopathies and atrial fibrillation, which may create an opportunity for the development of new therapeutic agents. Here we review the recent evidence for a role of NLRP3 inflammasome in the cardiomyocytes and discuss its potential role in the evolution of cardiac remodeling and arrhythmias and new opportunities created by these very recent developments.
format Online
Article
Text
id pubmed-6100656
institution National Center for Biotechnology Information
language English
publishDate 2018
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-61006562018-08-27 Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications Chen, Gong Chelu, Mihail G. Dobrev, Dobromir Li, Na Front Physiol Physiology Inflammasomes are high molecular weight protein complexes in the cytosol of immune and other cells that play a critical role in the innate immune system in response to cellular stress. NLRP3 inflammasome, the best-understood inflammasome, is known to mediate the maturation (activation) of caspase-1 from pro-caspase-1, causing the maturation and release of cytokines (e.g., interleukin-1β) and potentially leading to a form of inflammatory programmed cell death called pyroptosis. Previous work has shown that the NLRP3 components are expressed in cardiomyocytes and cardiac fibroblasts and recent studies have identified the NLRP3 inflammasome as a key nodal point in the pathogenesis of cardiomyopathies and atrial fibrillation, which may create an opportunity for the development of new therapeutic agents. Here we review the recent evidence for a role of NLRP3 inflammasome in the cardiomyocytes and discuss its potential role in the evolution of cardiac remodeling and arrhythmias and new opportunities created by these very recent developments. Frontiers Media S.A. 2018-08-13 /pmc/articles/PMC6100656/ /pubmed/30150941 http://dx.doi.org/10.3389/fphys.2018.01115 Text en Copyright © 2018 Chen, Chelu, Dobrev and Li. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Chen, Gong
Chelu, Mihail G.
Dobrev, Dobromir
Li, Na
Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications
title Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications
title_full Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications
title_fullStr Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications
title_full_unstemmed Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications
title_short Cardiomyocyte Inflammasome Signaling in Cardiomyopathies and Atrial Fibrillation: Mechanisms and Potential Therapeutic Implications
title_sort cardiomyocyte inflammasome signaling in cardiomyopathies and atrial fibrillation: mechanisms and potential therapeutic implications
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6100656/
https://www.ncbi.nlm.nih.gov/pubmed/30150941
http://dx.doi.org/10.3389/fphys.2018.01115
work_keys_str_mv AT chengong cardiomyocyteinflammasomesignalingincardiomyopathiesandatrialfibrillationmechanismsandpotentialtherapeuticimplications
AT chelumihailg cardiomyocyteinflammasomesignalingincardiomyopathiesandatrialfibrillationmechanismsandpotentialtherapeuticimplications
AT dobrevdobromir cardiomyocyteinflammasomesignalingincardiomyopathiesandatrialfibrillationmechanismsandpotentialtherapeuticimplications
AT lina cardiomyocyteinflammasomesignalingincardiomyopathiesandatrialfibrillationmechanismsandpotentialtherapeuticimplications