Evidence map›Paper›PMID 31779619›Full record

ArticleCardiovascular diabetology2019

Empagliflozin, a sodium glucose co-transporter-2 inhibitor, alleviates atrial remodeling and improves mitochondrial function in high-fat diet/streptozotocin-induced diabetic rats.

Qingmiao Shao, Lei Meng, Sharen Lee, Gary Tse, Mengqi Gong, Zhiwei Zhang, Jichao Zhao, Yungang Zhao, Guangping Li, Tong Liu

Registry-linked trialOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06342141 (Empagliflozin for Reducing the Risk of No-Reflow Phenomenon in Patients Undergoing Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction), which is not on this map. Cited by 183 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 10 pooled it
21.2field-weighted citation impact, top 1% 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.

NCT06342141 phase2active not recruitingnot on this mapstarted 2024, after this paper: background citation

Empagliflozin for Reducing the Risk of No-Reflow Phenomenon in Patients Undergoing Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction

TypeinterventionalSponsorInstituto Nacional de Cardiologia Ignacio ChavezRan2024 to 2026Enrolled162ConditionsSTEMI, No-Reflow PhenomenonArmsEmpagliflozin 25 milgrams (Mg), Empagliflozin 10 Mg
3 · Its place in the literature

Who cites it

183 citing papers in PubMed, 10 syntheses or guidelines pooled it, 286 citations in OpenAlex.

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  13. ELUCIDATE Trial: A Single-Center Randomized Controlled Study.Journal of the American Heart Association · 2024
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  15. Cardioprotective effects of Sodium-Glucose cotransporter-2 inhibitors in patients undergoing ventricular tachycardia (VT) ablation: a propensity-matched cohort study.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2026
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123 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 2 countries.

Qingmiao ShaoTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
Lei MengTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
Sharen LeeLaboratory of Cardiovascular Physiology, Li Ka Shing Institute of Health Sciences, Sha Tin, Hong Kong S.A.R., China.
Gary TseTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
Mengqi GongTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
Zhiwei ZhangTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China.
Jichao ZhaoAuckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand.
Yungang ZhaoTianjin Key Laboratory of Exercise Physiology and Sports Medicine, Department of Health & Exercise Science, Tianjin University of Sport, Tianjin, 300381, People's Republic of China.
Guangping LiTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China. tic_tjcardiol@126.com.
Tong LiuTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, 300211, People's Republic of China. liutongdoc@126.com.ORCID 0000-0003-0482-0738
Second Hospital of Tianjin Medical University · CNTianjin University of Sport · CNUniversity of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes mellitus is an important risk factor for atrial fibrillation (AF) development. Sodium-glucose co-transporter-2 (SGLT-2) inhibitors are used for the treatment of type 2 diabetes mellitus (T2DM). Their cardioprotective effects have been reported but whether they prevent AF in T2DM patients are less well-explored. We tested the hypothesis that the SGLT-2 inhibitor, empagliflozin, can prevent atrial remodeling in a diabetic rat model.

methodsHigh-fat diet and low-dose streptozotocin (STZ) treatment were used to induce T2DM. A total of 96 rats were randomized into the following four groups: (i) control (ii) T2DM, (iii) low-dose empagliflozin (10 mg/kg/day)/T2DM; and (iv) high-dose empagliflozin (30 mg/kg/day)/T2DM by the intragastric route for 8 weeks.

resultsCompared with the control group, left atrial diameter, interstitial fibrosis and the incidence of AF inducibility were significantly increased in the DM group. Moreover, atrial mitochondrial respiratory function, mitochondrial membrane potential, and mitochondrial biogenesis were impaired. Empagliflozin treatment significantly prevented the development of these abnormalities in DM rats, likely via the peroxisome proliferator-activated receptor-c coactivator 1α (PGC-1α)/nuclear respiratory factor-1 (NRF-1)/mitochondrial transcription factor A (Tfam) signaling pathway.

conclusionsEmpagliflozin can ameliorate atrial structural and electrical remodeling as well as improve mitochondrial function and mitochondrial biogenesis in T2DM, hence may be potentially used in the prevention of T2DM-related atrial fibrillation.

Indexed as

AnimalsAtrial FibrillationAtrial Function, LeftAtrial RemodelingBenzhydryl CompoundsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalGlucosidesHeart RateMaleMembrane Potential, MitochondrialMitochondria, HeartMitochondrial ProteinsOrganelle BiogenesisBenzhydryl CompoundsempagliflozinGlucosidesMitochondrial ProteinsSodium-Glucose Transporter 2 InhibitorsStreptozocinAtrial fibrillationAtrial remodelingDiabetic ratsEmpagliflozinMitochondrial functionSGLT-2 inhibitor

Identifiers

PMID31779619
PMCPMC6882319
OpenAlexW2989603136

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.