NIMA-Related Kinase-7 Activates Atrial Cardiomyocyte NLRP3 Inflammasome and Associates With Occurrence of Postoperative Atrial Fibrillation

Q: What is the clinical evidence from this study?

Study design: Case-Control. Population: Postoperative atrial fibrillation (n=79). Intervention: Development of postoperative atrial fibrillation vs. Maintenance of sinus rhythm (Controls). Primary outcome: Atrial NEK7 protein levels, NEK7-NLRP3 interaction, and caspase activity.

Q: What does this research mean for the field?

NIMA-related kinase-7 (NEK7) activates the NLRP3 inflammasome in atrial cardiomyocytes and associates with the occurrence of postoperative atrial fibrillation. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Issam Abu-Taha; Theresa Poppenborg; Florian Bruns; Marcel A. Tekook; Friederike Lunemann; Lisa Oehlke; Pascal Martsch; Markus Kamler; Payam Akhyari; Anke C. Fender; Samuel C. Dudley; Na Li; Dobromir Dobrev

doi:10.1161/circep.126.015003

October 7, 2026Circulation Arrhythmia and ElectrophysiologyOpen Access

NIMA-Related Kinase-7 Activates Atrial Cardiomyocyte NLRP3 Inflammasome and Associates With Occurrence of Postoperative Atrial Fibrillation

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Key result

Higher atrial NEK7 levels and NLRP3 interactions are linked to postoperative atrial fibrillation.

n=79

Why the study?

The upstream regulators of proarrhythmic inflammation in atrial cardiomyocytes and their role in postoperative atrial fibrillation are poorly understood.

Does elevated NEK7 expression drive NLRP3 inflammasome activation in atrial cardiomyocytes of patients developing postoperative atrial fibrillation?

Key Points

To determine whether NEK7 is required for NLRP3 inflammasome activation in atrial cardiomyocytes and contributes to susceptibility to postoperative atrial fibrillation.
Analyzed right-atrial appendages from open-heart surgery patients who maintained sinus rhythm (Ctl, n=43) versus those who developed postoperative atrial fibrillation (n=36).
Assessed causal signaling mechanisms in mouse HL-1 atrial cardiomyocytes using adenoviral NEK7 overexpression and CRISPR/Cas9-mediated NEK7 knockout stimulated with IL-1β (1 ng/ml) and nigericin (5 μmol/L).
Right-atrial tissue from patients prone to postoperative atrial fibrillation showed higher NEK7 protein levels, enhanced NEK7-NLRP3 protein interaction, increased NEK7-NLRP3 speck formation, higher caspase-4/5 activity, and increased IL-18 levels compared to sinus rhythm controls.
In mouse atrial cardiomyocytes, inflammatory priming with IL-1β plus nigericin increased NEK7-NLRP3 binding and upregulated pro-caspase-11 and cleaved caspase-11 levels, effects that were abolished by NEK7 knockout.

Study Design

Type

Case-Control (n=79)

Multicenter

No

Structured PICO

Does elevated NEK7 expression drive NLRP3 inflammasome activation in atrial cardiomyocytes of patients developing postoperative atrial fibrillation?

P

Population

79 patients undergoing open-heart surgery (36 who developed postoperative atrial fibrillation and 43 who remained in sinus rhythm), with a mean age of 66.6 years and 29% female.

E

Exposure

Postoperative atrial fibrillation (poAF) status and in vitro NEK7 overexpression/knockout

C

Comparator

Maintenance of sinus rhythm (controls) and wild-type/baseline NEK7 conditions

O

Outcome

Atrial NEK7 protein levels, NEK7-NLRP3 protein-protein interaction, and caspase-4/5 activitysurrogate

NEK7 serves as a critical upstream regulator of the proarrhythmic NLRP3 inflammasome in postoperative atrial fibrillation, suggesting the NEK7-NLRP3 axis as a potential novel therapeutic target.

Limitations

Future work is needed to dissect the differential regulation of caspase-1 and caspase-4/5/11 in atrial cardiomyocytes.
The role of NEK7 in other forms of atrial fibrillation requires validation.
Need to dissect differential regulation of caspase-1 and caspase-4/5/11 in Atrial-CM
Need to validate the role of NEK7 in other forms of AF

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Implication

NEK7 elevation may promote postoperative AF via NLRP3; hypothesis-generating for targeted therapies, requires prospective validation.

Abstract

Although inflammatory-signaling has emerged as a novel unifying-principle of atrial fibrillation (AF), the upstream regulators of proarrhythmic inflammation in atrial cardiomyocytes (Atrial-CM) are poorly understood(1–2). Postoperative AF (poAF) is a common complication after open-heart surgery driven largely by enhanced proinflammatory-signaling through NLRP3 (NACHT, LRR and PYD domains-binding protein-3) inflammasome(3). NEK7 (NIMA-related kinase-7) critically controls the oligomerization (activation) of NLRP3-inflammasome components in immune cells(4), with unknown roles in atrial arrhythmogenesis. Here, we determined whether NEK7 is required for NLRP3-inflammasome activation in Atrial-CM and poAF-prone patients.

Discussion

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Cite This Study

Abu-Taha et al. (2026) conducted a case-control in Postoperative atrial fibrillation (n=79). Development of postoperative atrial fibrillation vs. Maintenance of sinus rhythm (Controls) was evaluated on Atrial NEK7 protein levels, NEK7-NLRP3 interaction, and caspase activity. Patients prone to postoperative atrial fibrillation exhibited higher atrial NEK7 protein levels and a stronger NEK7-NLRP3 interaction compared to controls, driving proarrhythmic inflammasome activation.

synapsesocial.com/papers/6acc29b9005c34d980820f03 https://doi.org/10.1161/circep.126.015003

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NIMA-Related Kinase-7 Activates Atrial Cardiomyocyte NLRP3 Inflammasome and Associates With Occurrence of Postoperative Atrial Fibrillation

Key Points

Study Design

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

NIMA-Related Kinase-7 Activates Atrial Cardiomyocyte NLRP3 Inflammasome and Associates With Occurrence of Postoperative Atrial Fibrillation

Key Points

Study Design

Structured PICO

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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