Evidence map›Paper›PMID 32116783›Full record

ArticleFrontiers in physiology2020

Elevated β1-Adrenergic Receptor Autoantibody Levels Increase Atrial Fibrillation Susceptibility by Promoting Atrial Fibrosis.

Luxiang Shang, Ling Zhang, Mengjiao Shao, Min Feng, Jia Shi, Zhenyu Dong, Qilong Guo, Jiasuoer Xiaokereti, Ran Xiang, Huaxin Sun and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2020. 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
1.6field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Observational
  2. Review
  3. B cells promote atrial fibrillation via autoantibodies.Nature cardiovascular research · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. A novel vaccine targeting β1-adrenergic receptor.Hypertension research : official journal of the Japanese Society of Hypertension · 2023
    Article
  9. Article
  10. Autoantibodies in Atrial Fibrillation-State of the Art.International journal of molecular sciences · 2023
    Review
  11. Immune remodeling and atrial fibrillation.Frontiers in physiology · 2022
    Review
  12. Biased activation of βCell death discovery · 2021
    Article
  13. 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

12 authors at 2 institutions in 1 country.

Luxiang ShangDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Ling ZhangInstitute of Clinical Medical Research, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Mengjiao ShaoDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Min FengDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Jia ShiDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Zhenyu DongDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Qilong GuoDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Jiasuoer XiaokeretiDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Ran XiangDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Huaxin SunDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Xianhui ZhouDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Baopeng TangDepartment of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
First Affiliated Hospital of Xinjiang Medical University · CNXinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveBeta 1-adrenergic receptor autoantibodies (β1ARAbs) have been identified as a pathogenic factor in atrial fibrillation (AF), but the underlying pathogenetic mechanism is not well understood. We assessed the hypothesis that elevated β1ARAb levels increase AF susceptibility by promoting atrial fibrosis.

methodsA total of 70 patients with paroxysmal AF were continuously recruited. The serum levels of β1ARAb and circulating fibrosis biomarkers were analyzed by ELISA. Linear regression was used to examine the correlations of β1ARAb levels with left atrial diameter (LAD) and circulating fibrosis biomarker levels. Furthermore, we established a rabbit β1ARAb overexpression model. We conducted electrophysiological studies and multielectrode array recordings to evaluate the atrial effective refractory period (AERP), AF inducibility and electrical conduction. AF was defined as irregular, rapid atrial beats > 500 bpm for > 1000 ms. Echocardiography, hematoxylin and eosin staining, Masson's trichrome staining, and picrosirius red staining were performed to evaluate changes in atrial structure and detect fibrosis. Western blotting and PCR were used to detect alterations in the protein and mRNA expression of TGF-β1, collagen I and collagen III.

resultsPatients with a LAD ≥ 40 mm had higher β1ARAb levels than patients with a smaller LAD (8.87 ± 3.16 vs. 6.75 ± 1.34 ng/mL,

conclusionOur clinical and experiential studies showed that β1ARAbs participate in the development of AF and that the potential mechanism is related to the promotion of atrial fibrosis.

Indexed as

atrial fibrillationatrial fibrosisautoimmunecirculating fibrosis biomarkerβ1-adrenergic receptor autoantibody

Identifiers

PMID32116783
PMCPMC7028693
OpenAlexW3006386263

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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.