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Immunomodulation of the NLRP3 Inflammasome in Atherosclerosis, Coronary Artery Disease, and Acute Myocardial Infarction

Cardiovascular disease (CVD) remains the leading cause of mortality and morbidity worldwide. Atherosclerosis is responsible for the majority of cardiovascular disorders with inflammation as one of its driving processes. The nucleotide-binding oligomerization domain-like receptor family pyrin domain...

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Autores principales: Silvis, Max J. M., Demkes, Evelyne J., Fiolet, Aernoud T. L., Dekker, Mirthe, Bosch, Lena, van Hout, Gerardus P. J., Timmers, Leo, de Kleijn, Dominique P. V.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7892681/
https://www.ncbi.nlm.nih.gov/pubmed/32648087
http://dx.doi.org/10.1007/s12265-020-10049-w
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author Silvis, Max J. M.
Demkes, Evelyne J.
Fiolet, Aernoud T. L.
Dekker, Mirthe
Bosch, Lena
van Hout, Gerardus P. J.
Timmers, Leo
de Kleijn, Dominique P. V.
author_facet Silvis, Max J. M.
Demkes, Evelyne J.
Fiolet, Aernoud T. L.
Dekker, Mirthe
Bosch, Lena
van Hout, Gerardus P. J.
Timmers, Leo
de Kleijn, Dominique P. V.
author_sort Silvis, Max J. M.
collection PubMed
description Cardiovascular disease (CVD) remains the leading cause of mortality and morbidity worldwide. Atherosclerosis is responsible for the majority of cardiovascular disorders with inflammation as one of its driving processes. The nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, responsible for the release of the pro-inflammatory cytokines, interleukin-1β (IL-1β), and interleukin-18 (IL-18), has been studied extensively and showed to play a pivotal role in the progression of atherosclerosis, coronary artery disease (CAD), and myocardial ischemia reperfusion (I/R) injury. Both the NLRP3 inflammasome and its downstream cytokines, IL-1ß and IL-18, could therefore be promising targets in cardiovascular disease. This review summarizes the role of the NLRP3 inflammasome in atherosclerosis, CAD, and myocardial I/R injury. Furthermore, the current therapeutic approaches targeting the NLRP3 inflammasome and its downstream signaling cascade in atherosclerosis, CAD, and myocardial I/R injury are discussed.
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spelling pubmed-78926812021-03-15 Immunomodulation of the NLRP3 Inflammasome in Atherosclerosis, Coronary Artery Disease, and Acute Myocardial Infarction Silvis, Max J. M. Demkes, Evelyne J. Fiolet, Aernoud T. L. Dekker, Mirthe Bosch, Lena van Hout, Gerardus P. J. Timmers, Leo de Kleijn, Dominique P. V. J Cardiovasc Transl Res Review Cardiovascular disease (CVD) remains the leading cause of mortality and morbidity worldwide. Atherosclerosis is responsible for the majority of cardiovascular disorders with inflammation as one of its driving processes. The nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, responsible for the release of the pro-inflammatory cytokines, interleukin-1β (IL-1β), and interleukin-18 (IL-18), has been studied extensively and showed to play a pivotal role in the progression of atherosclerosis, coronary artery disease (CAD), and myocardial ischemia reperfusion (I/R) injury. Both the NLRP3 inflammasome and its downstream cytokines, IL-1ß and IL-18, could therefore be promising targets in cardiovascular disease. This review summarizes the role of the NLRP3 inflammasome in atherosclerosis, CAD, and myocardial I/R injury. Furthermore, the current therapeutic approaches targeting the NLRP3 inflammasome and its downstream signaling cascade in atherosclerosis, CAD, and myocardial I/R injury are discussed. Springer US 2020-07-09 2021 /pmc/articles/PMC7892681/ /pubmed/32648087 http://dx.doi.org/10.1007/s12265-020-10049-w Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Review
Silvis, Max J. M.
Demkes, Evelyne J.
Fiolet, Aernoud T. L.
Dekker, Mirthe
Bosch, Lena
van Hout, Gerardus P. J.
Timmers, Leo
de Kleijn, Dominique P. V.
Immunomodulation of the NLRP3 Inflammasome in Atherosclerosis, Coronary Artery Disease, and Acute Myocardial Infarction
title Immunomodulation of the NLRP3 Inflammasome in Atherosclerosis, Coronary Artery Disease, and Acute Myocardial Infarction
title_full Immunomodulation of the NLRP3 Inflammasome in Atherosclerosis, Coronary Artery Disease, and Acute Myocardial Infarction
title_fullStr Immunomodulation of the NLRP3 Inflammasome in Atherosclerosis, Coronary Artery Disease, and Acute Myocardial Infarction
title_full_unstemmed Immunomodulation of the NLRP3 Inflammasome in Atherosclerosis, Coronary Artery Disease, and Acute Myocardial Infarction
title_short Immunomodulation of the NLRP3 Inflammasome in Atherosclerosis, Coronary Artery Disease, and Acute Myocardial Infarction
title_sort immunomodulation of the nlrp3 inflammasome in atherosclerosis, coronary artery disease, and acute myocardial infarction
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7892681/
https://www.ncbi.nlm.nih.gov/pubmed/32648087
http://dx.doi.org/10.1007/s12265-020-10049-w
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