The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Enhanced Cardiomyocyte NLRP3 Inflammasome Signaling Promotes Atrial Fibrillation
Open accessAbstract
Background: Atrial fibrillation (AF) is frequently associated with enhanced inflammatory response. The NLRP3 (NACHT, LRR, and PYD domain containing protein 3) inflammasome mediates caspase-1 activation and interleukin-1β release in immune cells but is not known to play a role in cardiomyocytes (CMs). Here, we assessed the role of CM NLRP3 inflammasome in AF. Methods: NLRP3 inflammasome activation was assessed by immunoblot in atrial whole-tissue lysates and CMs from patients with paroxysmal AF or long-standing persistent (chronic) AF. To determine whether CM-specific activation of NLPR3 is sufficient to promote AF, a CM-specific knockin mouse model expressing constitutively active NLRP3 (CM-KI) was established. In vivo electrophysiology was used to assess atrial arrhythmia vulnerability. To evaluate the mechanism of AF, electric activation pattern, Ca 2+ spark frequency, atrial effective refractory period, and morphology of atria were evaluated in CM-KI mice and wild-type littermates. Results: NLRP3 inflammasome activity was increased in the atrial CMs of patients with paroxysmal AF and chronic AF. CM-KI mice developed spontaneous premature atrial contractions and inducible AF, which was attenuated by a specific NLRP3 inflammasome inhibitor, MCC950. CM-KI mice exhibited ectopic activity, abnormal sarcoplasmic reticulum Ca 2+ release, atrial effective refractory period shortening, and atrial hypertrophy. Adeno-associated virus subtype-9–mediated CM-specific knockdown of Nlrp3 suppressed AF development in CM-KI mice. Finally, genetic inhibition of Nlrp3 prevented AF development in CREM transgenic mice, a well-characterized mouse model of spontaneous AF. Conclusions: Our study establishes a novel pathophysiological role for CM NLRP3 inflammasome signaling, with a mechanistic link to the pathogenesis of AF, and establishes the inhibition of NLRP3 as a potential novel AF therapy approach.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease
Ridker, P. M., Everett, B. M., Thuren, T., MacFadyen, J. G., Chang, W. H., Ballantyne, C., Fonseca, F., Nicolau, J., Koenig, W., Anker, S. D., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1707914 · Cited by 9,482
Martinon, F., Burns, K., & Tschopp, J. (2002) · Molecular Cell · doi:10.1016/s1097-2765(02)00599-3 · Cited by 6,066
Gout-associated uric acid crystals activate the NALP3 inflammasome
Martinon, F., Pétrilli, V., Mayor, A., Tardivel, A., & Tschopp, J. (2006) · Nature · doi:10.1038/nature04516 · Cited by 5,326
A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases
Coll, R. C., Robertson, A. A. B., Chae, J. J., Higgins, S. C., Muñoz-Planillo, R., Inserra, M. C., Vetter, I., Dungan, L. S., Monks, B. G., Stutz, A., et al. (2015) · Nature Medicine · doi:10.1038/nm.3806 · Cited by 2,849
Inflammation as a risk factor for atrial fibrillation
Aviles, R. J., Martin, D. O., Apperson-Hansen, C., Houghtaling, P. L., Rautaharju, P., Kronmal, R. A., Tracy, R. P., Van Wagoner, D. R., Psaty, B. M., Lauer, M. S., et al. (2003) · Circulation · doi:10.1161/01.cir.0000103131.70301.4f · Cited by 1,425 · cited 1×
“13,14 Activation of the NLRP3 inflammasome requires 2 processes: (1) a priming event that induces transcription of NLRP3 and precursor caspase-1 (pro-Casp1) via toll-like receptor NFκB signaling, and (2) a subsequent triggering mechanism that promotes the assembly of NLRP3, adaptor-protein apoptosis-associated speck-l…”
MethodInflammasomes and Their Roles in Health and Disease
Lamkanfi, M., & Dixit, V. M. (2012) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-101011-155745 · Cited by 935
Inflammasome-mediated disease animal models reveal roles for innate but not adaptive immunity
Brydges, S. D., Mueller, J. L., McGeough, M. D., Pena, C. A., Misaghi, A., Gandhi, C., Putnam, C. D., Boyle, D. L., Firestein, G. S., Horner, A. A., et al. (2009) · Immunity · doi:10.1016/j.immuni.2009.05.005 · Cited by 339
DAMPs as mediators of sterile inflammation in aging-related pathologies
Feldman, N., Rotter-Maskowitz, A., & Okun, E. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.01.003 · Cited by 283
Aschar-Sobbi, R., Izaddoustdar, F., Korogyi, A. S., Wang, Q., Farman, G. P., Yang, F., Yang, W., Dorian, D., Simpson, J. A., Tuomi, J. M., et al. (2015) · Nature Communications · doi:10.1038/ncomms7018 · Cited by 185
Self-citation
Cited by
Joglar, J. A., Chung, M. K., Armbruster, A. L., Benjamin, E. J., Chyou, J. Y., Cronin, E. M., Deswal, A., Eckhardt, L. L., Goldberger, Z. D., Gopinathannair, R., et al. (2024) · Circulation · doi:10.1161/cir.0000000000001193 · Cited by 2,765
2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation
Joglar, J. A., Chung, M. K., Armbruster, A. L., Benjamin, E. J., Chyou, J. Y., Cronin, E. M., Deswal, A., Eckhardt, L. L., Goldberger, Z. D., Gopinathannair, R., et al. (2024) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2023.08.017 · Cited by 933
Postoperative atrial fibrillation: mechanisms, manifestations and management
Dobrev, D., Aguilar, M., Heijman, J., Guichard, J.-B., & Nattel, S. (2019) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0166-5 · Cited by 608
Self-citationBrundel, B. J. J. M., Ai, X., Hills, M. T., Kuipers, M. F., Lip, G. Y. H., & de Groot, N. M. S. (2022) · Nature Reviews Disease Primers · doi:10.1038/s41572-022-00347-9 · Cited by 499
Atrial Myocyte NLRP3/CaMKII Nexus Forms a Substrate for Postoperative Atrial Fibrillation
Heijman, J., Muna, A. P., Veleva, T., Molina, C. E., Sutanto, H., Tekook, M., Wang, Q., Abu-Taha, I. H., Gorka, M., Künzel, S., et al. (2020) · Circulation Research · doi:10.1161/circresaha.120.316710 · Cited by 292
Self-citation
Metadata
- Authors
- Yao, C., Veleva, T., Scott, L., Cao, S., Li, L., Chen, G., Jeyabal, P., Pan, X., Alsina, K. M., Abu-Taha, I., Ghezelbash, S., Reynolds, C. L., Shen, Y. H., LeMaire, S. A., Schmitz, W., Müller, F. U., El-Armouche, A., Tony Eissa, N., Beeton, C., Nattel, S., Wehrens, X. H. T., Dobrev, D., & Li, N.
- Venue
- Circulation
- Published
- 2018-11-13
- Volume
- 138
- Issue
- 20
- Pages
- 2227-2242
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2804559696
- Cited by
- 653
- References
- 9
- FWCI
- 32.51
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Enhanced Cardiomyocyte NLRP3 Inflammasome Signaling Promotes Atrial Fibrillation. https://app.cochat.ai/papers/10.1161/circulationaha.118.035202
- The paper
- Yao, C., Veleva, T., Scott, L., Cao, S., Li, L., Chen, G., Jeyabal, P., Pan, X., Alsina, K. M., Abu-Taha, I., Ghezelbash, S., Reynolds, C. L., Shen, Y. H., LeMaire, S. A., Schmitz, W., Müller, F. U., El-Armouche, A., Tony Eissa, N., Beeton, C., . . . Li, N. (2018). Enhanced Cardiomyocyte NLRP3 Inflammasome Signaling Promotes Atrial Fibrillation. Circulation. https://doi.org/10.1161/circulationaha.118.035202
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
