Evidence map›Paper›PMID 40145839›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

A Novel Protein NAB1-356 Encoded by circRNA circNAB1 Mitigates Atrial Fibrillation by Reducing Inflammation and Fibrosis.

William W Du, Muhammad Rafiq, Hui Yuan, Xiangmin Li, Sheng Wang, Jun Wu, Jinfeng Wei, Ren-Ke Li, Huiming Guo, Burton B Yang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

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  8. Single-cell Profiling Reveals Cooperative Participation ofInternational journal of medical sciences · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

William W DuSunnybrook Research Institute, and Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, M4N3M5, Canada.
Muhammad RafiqSunnybrook Research Institute, and Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, M4N3M5, Canada.
Hui YuanSunnybrook Research Institute, and Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, M4N3M5, Canada.
Xiangmin LiSunnybrook Research Institute, and Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, M4N3M5, Canada.
Sheng WangDepartment of Anesthesiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, 100029, China.
Jun WuToronto General Research Institute, University Health Network, Department of Physiology, University of Toronto, Toronto, M5G 2C4, Canada.
Jinfeng WeiDepartment of Anesthesiology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, 510080, China.
Ren-Ke LiToronto General Research Institute, University Health Network, Department of Physiology, University of Toronto, Toronto, M5G 2C4, Canada.
Huiming GuoDepartment of Anesthesiology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital & Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, 510080, China.
Burton B YangSunnybrook Research Institute, and Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, M4N3M5, Canada.ORCID https://orcid.org/0000-0002-2892-7209

Funding

CIHR PJT-153105CIHR PJT-155962
6 · The paper itself

Abstract

Atrial fibrillation (AF) is a common arrhythmia with irregular atrial electrical activity. Circular RNAs (circRNAs) are key regulators in tissue homeostasis, yet their role in AF remains unclear. Here, we investigated the expression and function of circNAB1 in AF using high-throughput sequencing and functional assays in circNAB1 transgenic mice. We identified circNAB1 as a significantly downregulated circRNA in AF patient specimens. Silencing circNAB1 promoted collagen deposition and inflammation, whereas overexpression reduces atrial fibrosis and AF susceptibility in mice, consistent with results observed in human atrial tissues. Mechanistically, circNAB1 translates into a novel protein, NAB1-356, which is highly expressed in human cardiac hypertrophy. NAB1-356 interacts with EGR1 as NAB1 does, decreasing fibrosis and inflammation in the atrium. Furthermore, NAB1-356 also regulates transcription factor Runx1 and Gadd45b transcription, exerting regulatory effects on cytokine expression and fibrosis. Targeting EGR1, Gadd45b, and Runx1 by circNAB1 or siRNAs attenuate AF incidence and cardiac remodeling, suggesting potential therapeutic strategies for AF management. Delivery of circNAB1 improves AF conditions in LKB1 knockout mice, further highlighting its anti-arrhythmic potential. Our findings elucidate the mechanistic role of circNAB1 in AF pathogenesis and suggest its therapeutic implications for cardiac remodeling-associated disorders.

Indexed as

Atrial FibrillationInflammationRNA, CircularAnimalsDisease Models, AnimalFibrosisHeart AtriaHumansMaleMiceMice, TransgenicRNA, Circularcardiac fibrosiscardiac remodelingcircNAB1circular RNA

Identifiers

PMID40145839
PMCPMC12120700

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.