Evidence map›Paper›PMID 39730461›Full record

ArticleScientific reports2024

Effects of Empagliflozin and Dapagliflozin in alleviating cardiac fibrosis through SIRT6-mediated oxidative stress reduction.

Hong-Xia Ma, Ke Wu, Fei-Hong Dong, Bing-Kun Cai, Di Wu, Hui-Yi Lu

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Article
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  7. Article
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  11. Review
  12. Rewiring the scar: translational advances in cardiac fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  13. Cardiac fibrosis: from mechanisms and models to medicines.Trends in pharmacological sciences · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Gliflozins in hypertension: basic mechanisms and clinical insights.American journal of physiology. Renal physiology · 2025
    Review
  19. Review
  20. 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

6 authors.

Hong-Xia Ma *Department of Pharmacy, The Second Affiliated Hospital of Dalian Medical University, #467 Zhongshan Road, Dalian, 116023, Liaoning, China.
Ke Wu *Department of Pharmacy, The Second Affiliated Hospital of Dalian Medical University, #467 Zhongshan Road, Dalian, 116023, Liaoning, China.
Fei-Hong DongDepartment of Pharmacy, The Second Affiliated Hospital of Dalian Medical University, #467 Zhongshan Road, Dalian, 116023, Liaoning, China.
Bing-Kun CaiDepartment of Pharmacy, The Second Affiliated Hospital of Dalian Medical University, #467 Zhongshan Road, Dalian, 116023, Liaoning, China.
Di WuDepartment of Pharmacy, The Second Affiliated Hospital of Dalian Medical University, #467 Zhongshan Road, Dalian, 116023, Liaoning, China. dw_0615@dmu.edu.cn.
Hui-Yi LuDepartment of Pharmacy, The Second Affiliated Hospital of Dalian Medical University, #467 Zhongshan Road, Dalian, 116023, Liaoning, China. huiyi-l@dmu.edu.cn.

Funding

Dalian Key Field Innovation Team Project 2021RT14Dalian Medical Science Research Project 22Z12006Dalian Science and Technology Innovation Fund 2023RQ010National Natural Science Foundation of China 82204387
6 · The paper itself

Abstract

Sodium-glucose co-transport protein 2 (SGLT2) inhibitors, a novel category of oral hypoglycemic agents, offer a promising outlook for individuals experiencing heart failure with reduced ejection fraction. Evidence is emerging that highlights their potential in alleviating myocardial fibrosis and oxidative stress. However, the precise mechanisms through which SGLT2 inhibitors influence myocardial fibrosis induced by angiotensin II (Ang II) or transforming growth factor-β1 (TGF-β1) are not fully understood. This study aims to explore the intricate mechanisms by which SGLT2 inhibitors ameliorate myocardial fibrosis, particularly focusing on the nuanced interplay within the SIRT6 signaling pathway. Primary cardiac fibroblasts were isolated from the hearts of 1-3-day-old neonatal KM mice, were stimulated with Ang II or TGF-β1 to establish an in vitro model of myocardial fibrosis. Treatment with 10 µM Empagliflozin (EMPA) and Dapagliflozin (DAPA) significantly curtailed the proliferation of cardiac fibroblasts, substantially reduced collagen expression induced by Ang II/TGF-β1, and mitigated the phenotypic transformation and oxidative stress response. SIRT6, which is closely associated with myocardial fibrosis, demonstrated that the suppression its expression attenuated the protective effects of EMPA and DAPA against myocardial fibrosis and oxidative stress. Our findings suggest that SGLT2 inhibitors markedly decrease the Ang II/TGF-β1-induced transformation of cardiac fibroblasts to a myofibroblast phenotype by upregulating SIRT6 protein expression, thereby inhibiting oxidative stress and ameliorating myocardial fibrosis.

Indexed as

Benzhydryl CompoundsFibrosisGlucosidesOxidative StressSirtuinsSodium-Glucose Transporter 2 InhibitorsTransforming Growth Factor beta1Angiotensin IIAnimalsCell ProliferationFibroblastsMiceMyocardiumSignal TransductionAngiotensin IIBenzhydryl CompoundsdapagliflozinempagliflozinGlucosidesSirt6 protein, mouseSirtuinsSodium-Glucose Transporter 2 InhibitorsTransforming Growth Factor beta1DapagliflozinEmpagliflozinMyocardial fibrosisOxidative stress injurySIRT6

Identifiers

PMID39730461
PMCPMC11680569

What OpenQuestion holds

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Registered trials

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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.