Evidence map›Paper›PMID 36304536›Full record

ArticleFrontiers in cardiovascular medicine2022

Cardiac-specific knockdown of Bhlhe40 attenuates angiotensin II (Ang II)-Induced atrial fibrillation in mice.

Kai-Wen Ren, Xiao-Hong Yu, Yu-Hui Gu, Xin Xie, Yu Wang, Shi-Hao Wang, Hui-Hua Li, Hai-Lian Bi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.6field-weighted citation impact, top 6% of its field
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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Immune Regulation in Atrial Cardiomyopathy.Reviews in cardiovascular medicine · 2025
    Review
  5. Article
  6. Article
  7. IGF-II regulates lysyl oxidase propeptide and mediates its effects in part via basic helix-loop-helix E40.Matrix biology : journal of the International Society for Matrix Biology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Ubiquitin-specific protease 38 promotes inflammatory atrial fibrillation induced by pressure overload.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023
    Article
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

8 authors at 3 institutions in 1 country.

Kai-Wen RenInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Xiao-Hong YuDepartment of Cardiology, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Yu-Hui GuInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Xin XieInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Yu WangInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Shi-Hao WangInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Hui-Hua LiDepartment of Emergency Medicine, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Hai-Lian BiInstitute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, Dalian, China.
First Affiliated Hospital of Dalian Medical University · CNDalian Medical University · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrosis and atrial inflammation are associated with the pathogenesis of atrial fibrillation (AF). Basic helix-loop-helix family member E40 (Bhlhe40) is an important transcription factor, which is involved in tumors, inflammation, apoptosis, viral infection, and hypoxia. However, its role and molecular mechanism in AF remain unclear. In this study, a mouse model of AF was induced by Ang II infusion. The atrial diameter was evaluated using echocardiography. Induction and duration of AF were measured by programmed electrical stimulation. Atrial structural remodeling was detected using routine histologic examinations. Our results showed that Bhlhe40 was significantly upregulated in angiotensin II (Ang II)-stimulated atrial cardiomyocytes and atrial tissues and in tissues from patients with AF. Cardiac-specific knockdown of Bhlhe40 in mice by a type 9 recombinant adeno-associated virus (rAAV9)-shBhlhe40 significantly ameliorated Ang II-induced atrial dilatation, atrial fibrosis, and atrial inflammation, as well as the inducibility and duration of AF. Mechanistically, cardiac-specific knockdown of Bhlhe40 attenuated Ang II-induced activation of NF-κB/NLRP3, TGF-1β/Smad2 signals, the increased expression of CX43, and the decreased expression of Kv4.3 in the atria. This is the first study to suggest that Bhlhe40 is a novel regulator of AF progression, and identifying Bhlhe40 may be a new therapeutic target for hypertrophic remodeling and heart failure.

Indexed as

atrial fibrillationatrial fibrosisatrial inflammationBhlhe40NLRP3

Identifiers

PMID36304536
PMCPMC9592817
OpenAlexW4304172687

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.