Evidence map›Paper›PMID 31910841›Full record

ArticleCardiovascular diabetology2020

Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?

Salva R Yurista, Herman H W Silljé, Michiel Rienstra, Rudolf A de Boer, B Daan Westenbrink

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

Article in Cardiovascular diabetology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 4 pooled it
5.4field-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

20 citing papers in PubMed, 4 syntheses or guidelines pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Article
  7. Article
  8. Review
  9. Article
  10. Amiodarone Therapy: Updated Practical Insights.Journal of clinical medicine · 2024
    Review
  11. Review
  12. Article
  13. Review
  14. A New Hope: Sodium-Glucose Cotransporter-2 Inhibition to Prevent Atrial Fibrillation.Journal of cardiovascular development and disease · 2022
    Review
  15. SGLT2 Inhibitors and Their Antiarrhythmic Properties.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Observational
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Salva R YuristaDepartment of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB, Groningen, The Netherlands.
Herman H W SilljéDepartment of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB, Groningen, The Netherlands.
Michiel RienstraDepartment of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB, Groningen, The Netherlands.
Rudolf A de BoerDepartment of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB, Groningen, The Netherlands.
B Daan WestenbrinkDepartment of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB, Groningen, The Netherlands. b.d.westenbrink@umcg.nl.
University of Groningen · NLUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While patients with type 2 diabetes mellitus (T2DM) are at increased risk to develop atrial fibrillation (AF), the mechanistic link between T2DM and AF-susceptibility remains unclear. Common co-morbidities of T2DM, particularly hypertension, may drive AF in the setting of T2DM. But direct mechanisms may also explain this relation, at least in part. In this regard, recent evidence suggests that mitochondrial dysfunction drives structural, electrical and contractile remodelling of atrial tissue in patients T2DM. Mitochondrial dysfunction may therefore be the mechanistic link between T2DM and AF and could also serve as a therapeutic target. An elegant series of experiments published in Cardiovascular Diabetology provide compelling new evidence to support this hypothesis. Using a model of high fat diet (HFD) and low-dose streptozotocin (STZ) injection, Shao et al. provide data that demonstrate a direct association between mitochondrial dysfunction and the susceptibility to develop AF. But the authors also demonstrated that the sodium-glucose co-transporter 2 inhibitors (SGLT2i) empagliflozin has the capacity to restore mitochondrial function, ameliorate electrical and structural remodelling and prevent AF. These findings provide a new horizon in which mitochondrial targeted therapies could serve as a new class of antiarrhythmic drugs.

Indexed as

Atrial FibrillationAtrial RemodelingDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2AnimalsBenzhydryl CompoundsDiet, High-FatGlucoseGlucosidesHumansMitochondriaRatsSodiumSodium-Glucose Transporter 2StreptozocinBenzhydryl CompoundsempagliflozinGlucoseGlucosidesSodiumSodium-Glucose Transporter 2StreptozocinAtrial fibrillationDiabetesMitochondriaSodium-glucose co-transporter-2 inhibitors

Identifiers

PMID31910841
PMCPMC6945755
OpenAlexW2999986417

What Socratic 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 Socratic graph.