Evidence map›Paper›PMID 34073033›Full record

ReviewInternational journal of molecular sciences2021

Implications of SGLT Inhibition on Redox Signalling in Atrial Fibrillation.

David Bode, Lukas Semmler, Christian U Oeing, Alessio Alogna, Gabriele G Schiattarella, Burkert M Pieske, Frank R Heinzel, Felix Hohendanner

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Managing arrhythmia in cardiac resynchronisation therapy.Frontiers in cardiovascular medicine · 2023
    Review
  8. Article
  9. Review
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 4 institutions in 2 countries.

David BodeCenter for Cardiovascular Research (CCR), Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum, Charité University Medicine, Augustenburgerplatz 1, 13353 Berlin, Germany.ORCID 0000-0003-4077-111X
Lukas SemmlerCenter for Cardiovascular Research (CCR), Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum, Charité University Medicine, Augustenburgerplatz 1, 13353 Berlin, Germany.
Christian U OeingCenter for Cardiovascular Research (CCR), Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum, Charité University Medicine, Augustenburgerplatz 1, 13353 Berlin, Germany.ORCID 0000-0002-0816-4443
Alessio AlognaCenter for Cardiovascular Research (CCR), Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum, Charité University Medicine, Augustenburgerplatz 1, 13353 Berlin, Germany.
Gabriele G SchiattarellaCenter for Cardiovascular Research (CCR), Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum, Charité University Medicine, Augustenburgerplatz 1, 13353 Berlin, Germany.
Burkert M PieskeCenter for Cardiovascular Research (CCR), Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum, Charité University Medicine, Augustenburgerplatz 1, 13353 Berlin, Germany.
Frank R HeinzelCenter for Cardiovascular Research (CCR), Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum, Charité University Medicine, Augustenburgerplatz 1, 13353 Berlin, Germany.
Felix HohendannerCenter for Cardiovascular Research (CCR), Department of Internal Medicine and Cardiology, Campus Virchow-Klinikum, Charité University Medicine, Augustenburgerplatz 1, 13353 Berlin, Germany.
German Centre for Cardiovascular Research · DEDeutsches Herzzentrum der Charité · DEGuy's and St Thomas' NHS Foundation Trust · GBMax Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atrial fibrillation (AF) is the most common sustained (atrial) arrhythmia, a considerable global health burden and often associated with heart failure. Perturbations of redox signalling in cardiomyocytes provide a cellular substrate for the manifestation and maintenance of atrial arrhythmias. Several clinical trials have shown that treatment with sodium-glucose linked transporter inhibitors (SGLTi) improves mortality and hospitalisation in heart failure patients independent of the presence of diabetes. Post hoc analysis of the DECLARE-TIMI 58 trial showed a 19% reduction in AF in patients with diabetes mellitus (hazard ratio, 0.81 (95% confidence interval: 0.68-0.95), n = 17.160) upon treatment with SGLTi, regardless of pre-existing AF or heart failure and independent from blood pressure or renal function. Accordingly, ongoing experimental work suggests that SGLTi not only positively impact heart failure but also counteract cellular ROS production in cardiomyocytes, thereby potentially altering atrial remodelling and reducing AF burden. In this article, we review recent studies investigating the effect of SGLTi on cellular processes closely interlinked with redox balance and their potential effects on the onset and progression of AF. Despite promising insight into SGLTi effect on Ca

Indexed as

Myocytes, CardiacAnimalsAtrial FibrillationCalciumCells, CulturedHumansOxidation-ReductionOxidative StressReactive Oxygen SpeciesSodium-Glucose Transporter 1Sodium-Glucose Transporter 2 InhibitorsCalciumReactive Oxygen SpeciesSLC5A1 protein, humanSodium-Glucose Transporter 1Sodium-Glucose Transporter 2 Inhibitorsatrial fibrillationCa2+ homeostasiscardiomyocytesheart failuremitochondrial functionoxidative stressreactive oxygen speciesredox signallingSGLT inhibition

Identifiers

PMID34073033
PMCPMC8198069
OpenAlexW3165541413

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.