Literature DB >> 33748830

Genetically determined NLRP3 inflammasome activation associates with systemic inflammation and cardiovascular mortality.

Stefan J Schunk1, Marcus E Kleber2,3, Winfried März2,4,5, Shichao Pang6, Stephen Zewinger1, Sarah Triem1, Philipp Ege1, Matthias C Reichert7, Marcin Krawczyk7,8, Susanne N Weber7, Isabella Jaumann1, David Schmit1, Tamim Sarakpi1, Stefan Wagenpfeil9, Rafael Kramann10,11, Eric Boerwinkle12,13, Christie M Ballantyne14,15, Megan L Grove12, Vinicius Tragante16, Anna P Pilbrow17, A Mark Richards17, Vicky A Cameron17, Robert N Doughty18, Marie-Pierre Dubé19,20, Jean-Claude Tardif19,20, Yassamin Feroz-Zada19, Maxine Sun20, Chang Liu21, Yi-An Ko22, Arshed A Quyyumi21, Jaana A Hartiala23, W H Wilson Tang24,25, Stanley L Hazen24,25, Hooman Allayee23, Caitrin W McDonough26, Yan Gong26, Rhonda M Cooper-DeHoff26,27, Julie A Johnson26,27, Markus Scholz28,29, Andrej Teren29,30, Ralph Burkhardt29,31, Andreas Martinsson32, J Gustav Smith33, Lars Wallentin34,35, Stefan K James34,35, Niclas Eriksson34,35, Harvey White36, Claes Held34,35, Dawn Waterworth37, Stella Trompet38, J Wouter Jukema39,40, Ian Ford41, David J Stott42, Naveed Sattar43, Sharon Cresci44,45, John A Spertus46, Hannah Campbell44,45, Sascha Tierling47, Jörn Walter47, Emmanuel Ampofo48, Barbara A Niemeyer49, Peter Lipp50, Heribert Schunkert6,51, Michael Böhm52, Wolfgang Koenig6,51,53, Danilo Fliser1, Ulrich Laufs54, Thimoteus Speer1,55.   

Abstract

AIMS: Inflammation plays an important role in cardiovascular disease (CVD) development. The NOD-like receptor protein-3 (NLRP3) inflammasome contributes to the development of atherosclerosis in animal models. Components of the NLRP3 inflammasome pathway such as interleukin-1β can therapeutically be targeted. Associations of genetically determined inflammasome-mediated systemic inflammation with CVD and mortality in humans are unknown. METHODS AND
RESULTS: We explored the association of genetic NLRP3 variants with prevalent CVD and cardiovascular mortality in 538 167 subjects on the individual participant level in an explorative gene-centric approach without performing multiple testing. Functional relevance of single-nucleotide polymorphisms on NLRP3 inflammasome activation has been evaluated in monocyte-enriched peripheral blood mononuclear cells (PBMCs). Genetic analyses identified the highly prevalent (minor allele frequency 39.9%) intronic NLRP3 variant rs10754555 to affect NLRP3 gene expression. rs10754555 carriers showed significantly higher C-reactive protein and serum amyloid A plasma levels. Carriers of the G allele showed higher NLRP3 inflammasome activation in isolated human PBMCs. In carriers of the rs10754555 variant, the prevalence of coronary artery disease was significantly higher as compared to non-carriers with a significant interaction between rs10754555 and age. Importantly, rs10754555 carriers had significantly higher risk for cardiovascular mortality during follow-up. Inflammasome inducers (e.g. urate, triglycerides, apolipoprotein C3) modulated the association between rs10754555 and mortality.
CONCLUSION: The NLRP3 intronic variant rs10754555 is associated with increased systemic inflammation, inflammasome activation, prevalent coronary artery disease, and mortality. This study provides evidence for a substantial role of genetically driven systemic inflammation in CVD and highlights the NLRP3 inflammasome as a therapeutic target. Published on behalf of the European Society of Cardiology. All rights reserved.
© The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.

Entities:  

Keywords:  Cardiovascular diseases; Coronary artery disease; Inflammasome; Inflammation; NLRP3

Mesh:

Substances:

Year:  2021        PMID: 33748830      PMCID: PMC8244638          DOI: 10.1093/eurheartj/ehab107

Source DB:  PubMed          Journal:  Eur Heart J        ISSN: 0195-668X            Impact factor:   29.983


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