Evidence map›Paper›PMID 36388109›Full record

ArticleFrontiers in physiology2022

A novel murine model of atrial fibrillation by diphtheria toxin-induced injury.

Theresa Trieu, Philbert Mach, Kaitlyn Bunn, Vincent Huang, Jamie Huang, Christine Chow, Haruko Nakano, Viviana M Fajardo, Marlin Touma, Shuxun Ren and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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 1 institution in 2 countries.

Theresa TrieuDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
Philbert MachDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
Kaitlyn BunnDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
Vincent HuangDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
Jamie HuangDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
Christine ChowDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
Haruko NakanoDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
Viviana M FajardoDepartment of Pediatrics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Marlin ToumaDepartment of Pediatrics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Shuxun RenDepartments of Anesthesiology, Physiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Yibin WangDepartments of Anesthesiology, Physiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Atsushi NakanoDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California, Los Angeles, Los Angeles, CA, United States.
University of California, Los Angeles · US

Funding

Metabolic regulation of heart formationR01HL142801 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI NAKANO, ATSUSHI · 2019 to 2022
$1.6M
NHLBI NIH HHS R01 HL142801
6 · The paper itself

Abstract

The treatment of atrial fibrillation (AF) continues to be a significant clinical challenge. While genome-wide association studies (GWAS) are beginning to identify AF susceptibility genes (Gudbjartsson et al., Nature, 2007, 448, 353-357; Choi et al., Circ. Res., 2020, 126, 200-209; van Ouwerkerk et al., Circ. Res., 2022, 127, 229-243), non-genetic risk factors including physical, chemical, and biological environments remain the major contributors to the development of AF. However, little is known regarding how non-genetic risk factors promote the pathogenesis of AF (Weiss et al., Heart Rhythm, 2016, 13, 1868-1877; Chakraborty et al., Heart Rhythm, 2020, 17, 1,398-1,404; Nattel et al., Circ. Res., 2020, 127, 51-72). This is, in part, due to the lack of a robust and reliable animal model induced by non-genetic factors. The currently available models using rapid pacing protocols fail to generate a stable AF phenotype in rodent models, often requiring additional genetic modifications that introduce potential sources of bias (Schüttler et al., Circ. Res., 2020, 127, 91-110). Here, we report a novel murine model of AF using an inducible and tissue-specific activation of diphtheria toxin (DT)-mediated cellular injury system. By the tissue-specific and inducible expression of human HB-EGF in atrial myocytes, we developed a reliable, robust and scalable murine model of AF that is triggered by a non-genetic inducer without the need for AF susceptibility gene mutations.

Indexed as

amiodaroneatrial fibrillationdiphtheria toxinnon-genetic causesarcolipin (SLN)

Identifiers

PMID36388109
PMCPMC9659601
OpenAlexW4307871217

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.