Evidence map›Paper›PMID 32717176›Full record

ReviewCirculation research2020

Inflammasomes and Proteostasis Novel Molecular Mechanisms Associated With Atrial Fibrillation.

Na Li, Bianca J J M Brundel

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 96 citations in OpenAlex.

  1. Differential effects of semaglutide and colchicine on atrial remodeling in rats with reduced ejection fraction after myocardial infarction.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 · 2026
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  10. [Pathogenesis and potential diagnostic biomarkers of atrial fibrillation in Chinese population: a study based on bioinfor-matics].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
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4 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Na LiFrom the Department of Medicine (Cardiovascular Research) (N.L.), Baylor College of Medicine, Houston, TX.
Bianca J J M BrundelDepartment of Physiology, Amsterdam UMC, Vrije Universiteit, Amsterdam Cardiovascular Sciences, the Netherlands (B.J.J.M.B.).
Amsterdam University Medical Centers · NLBaylor College of Medicine · US

Funding

Ryanodine receptor regulation in post-operative atrial fibrillationR01HL089598 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2007 to 2022
$6.5M
The Role of Inflammasome in the Pathogenesis of Atrial FibrillationR01HL136389 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Na Li · 2017 to 2026
$5.6M
Mechanisms underlying atrial fibrillation associated with chronic kidney diseaseR01HL147108 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI LI, NA, WEHRENS, XANDER H.T. · 2019 to 2022
$2.0M
Inflammasome mediated pathogenesis of atrial fibrillationR56HL131649 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI LI, NA · 2016 to 2016
$396k
NHLBI NIH HHS R01 HL089598NHLBI NIH HHS R01 HL136389NHLBI NIH HHS R01 HL147108NHLBI NIH HHS R56 HL131649
6 · The paper itself

Abstract

Atrial fibrillation (AF), the most common progressive and age-related cardiac arrhythmia, affects millions of people worldwide. AF is associated with common risk factors, including hypertension, diabetes mellitus, and obesity, and serious complications such as stroke and heart failure. Notably, AF is progressive in nature, and because current treatment options are mainly symptomatic, they have only a moderate effect on prevention of arrhythmia progression. Hereto, there is an urgent unmet need to develop mechanistic treatments directed at root causes of AF. Recent research findings indicate a key role for inflammasomes and derailed proteostasis as root causes of AF. Here, we elaborate on the molecular mechanisms of these 2 emerging key pathways driving the pathogenesis of AF. First the role of NLRP3 (NACHT, LRR, and PYD domains-containing protein 3) inflammasome on AF pathogenesis and cardiomyocyte remodeling is discussed. Then we highlight pathways of proteostasis derailment, including exhaustion of cardioprotective heat shock proteins, disruption of cytoskeletal proteins via histone deacetylases, and the recently discovered DNA damage-induced nicotinamide adenine dinucleotide

Indexed as

ProteostasisAnimalsAtrial FibrillationHumansInflammasomesInflammasomesatrial fibrillationDNA damagehistone deacetylasesinflammasomesinflammationproteostasis

Identifiers

PMID32717176
PMCPMC7388703
OpenAlexW3036295560

What OpenQuestion holds

Textmetadata
LicenceTDM
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.