Evidence map›Paper›PMID 30710997›Full record

ArticleCardiovascular diabetology2019

SGLT2 inhibition with empagliflozin attenuates myocardial oxidative stress and fibrosis in diabetic mice heart.

Chenguang Li, Jie Zhang, Mei Xue, Xiaoyu Li, Fei Han, Xiangyang Liu, Linxin Xu, Yunhong Lu, Ying Cheng, Ting Li and 3 more

2 registry-linked trialsOpen access · goldAbstract read
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 2 registered trials, which are not on this map. Cited by 344 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
344citing papers in PubMed, 6 pooled it
40.6field-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.

NCT05335629 nacompletedstarted 2022, after this paper: background citation

Evaluation of the Effect of Dapagliflozin on Cardiac Remodeling in Post Myocardial Infarction Patients

Ran2022Enrolled54Registered outcomes2Posted comparisons0ConditionsDiabetes Mellitus, Type 2, Myocardial Infarction, Myocardial Remodeling, VentricularArmsDapagliflozin 10mg Tab
Open the trial in the graph
NCT04792190 phase4completednot on this mapstarted 2021, after this paper: background citation

Use of Dapagliflozin to Reduce Burden of Atrial Fibrillation in Patients Undergoing Catheter Ablation of Symptomatic Atrial Fibrillation (DAPA-AF) Prospective, Randomized, Multicenter, Placebo-Controlled Trial

TypeinterventionalSponsorUniversity of RochesterRan2021 to 2023Enrolled25ConditionsAtrial FibrillationArmsdapagliflozin, Placebo
3 · Its place in the literature

Who cites it

344 citing papers in PubMed, 6 syntheses or guidelines pooled it, 572 citations in OpenAlex.

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  11. Impact of SGLT2 inhibitors in cardiac amyloidosis: A systematic review and meta-analysis.American heart journal plus : cardiology research and practice · 2026
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  18. Acute vascular redox modulation by SGLT2 inhibition in non-diabetic patients.Cardiovascular diabetology. Endocrinology reports · 2026
    Article
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284 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

13 authors at 1 institution in 1 country.

Chenguang LiNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Jie ZhangNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Mei XueNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Xiaoyu LiNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Fei HanNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Xiangyang LiuNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Linxin XuNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Yunhong LuNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Ying ChengNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Ting LiNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Xiaochen YuNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China.
Bei SunNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China. sun_peipei220@hotmail.com.
Liming ChenNHC Key Laboratory of Hormones and Development (Tianjin Medical University), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin, 300070, China. xfx22081@vip.163.com.
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHyperglycaemia associated with myocardial oxidative stress and fibrosis is the main cause of diabetic cardiomyopathy. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor has recently been reported to improve glycaemic control in patients with type 2 diabetes in an insulin-independent manner. The aim of this study was to investigate the effect of empagliflozin on myocardium injury and the potential mechanism in type 2 diabetic KK-Ay mice.

methodsThirty diabetic KK-Ay mice were administered empagliflozin (10 mg/kg/day) by oral gavage daily for 8 weeks. After 8 weeks, heart structure and function were evaluated by echocardiography. Oxidants and antioxidants were measured and cardiac fibrosis was analysed using immunohistochemistry, Masson's trichrome stain and Western blot.

resultsResults showed that empagliflozin improved diabetic myocardial structure and function, decreased myocardial oxidative stress and ameliorated myocardial fibrosis. Further study indicated that empagliflozin suppressed oxidative stress and fibrosis through inhibition of the transforming growth factor β/Smad pathway and activation of Nrf2/ARE signaling.

conclusionsGlycaemic control with empagliflozin significantly ameliorated myocardial oxidative stress injury and cardiac fibrosis in diabetic mice. Taken together, these results indicate that the empagliflozin is a promising agent for the prevention and treatment of diabetic cardiomyopathy.

Indexed as

AnimalsAntioxidant Response ElementsAntioxidantsBenzhydryl CompoundsDiabetes Mellitus, Type 2Diabetic CardiomyopathiesDisease Models, AnimalFibrosisGlucosidesMice, Inbred C57BLMyocardiumNF-E2-Related Factor 2Oxidative StressPhosphorylationSignal TransductionSmad ProteinsAntioxidantsBenzhydryl CompoundsempagliflozinGlucosidesNfe2l2 protein, mouseNF-E2-Related Factor 2Slc5a2 protein, mouseSmad ProteinsSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsTgfb1 protein, mouseTransforming Growth Factor beta1EmpagliflozinMyocardial fibrosisOxidative stressSGLT2Type 2 diabetes mellitus

Identifiers

PMID30710997
PMCPMC6359811
OpenAlexW2911996337

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.