Evidence map›Paper›PMID 36068525›Full record

ArticleBMC medicine2022

Dapagliflozin attenuates diabetes-induced diastolic dysfunction and cardiac fibrosis by regulating SGK1 signaling.

Seul-Gee Lee, Darae Kim, Jung-Jae Lee, Hyun-Ju Lee, Ro-Kyung Moon, Yong-Joon Lee, Seung-Jun Lee, Oh-Hyun Lee, Choongki Kim, Jaewon Oh and 7 more

Open access · goldAbstract read
In one paragraph

Article in BMC medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

35 citing papers in PubMed, 61 citations in OpenAlex.

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  16. SGLT2 inhibitors: how do they affect the cardiac cells.Molecular and cellular biochemistry · 2025
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  18. Article
  19. Anti-Inflammatory Effects of SGLT2 Inhibitors: Focus on Macrophages.International journal of molecular sciences · 2025
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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

17 authors at 3 institutions in 1 country.

Seul-Gee Lee *Yonsei Cardiovascular Research Institute, Yonsei University College of Medicine, Seoul, South Korea.
Darae Kim *Division of Cardiology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea.
Jung-Jae LeeYonsei Cardiovascular Research Institute, Yonsei University College of Medicine, Seoul, South Korea.
Hyun-Ju LeeGraduate Yonsei University, Seoul, South Korea.
Ro-Kyung MoonCollege of Medicine, Yonsei University Seoul, Seoul, South Korea.
Yong-Joon LeeDivision of Cardiology, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Seung-Jun LeeDivision of Cardiology, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Oh-Hyun LeeDivision of Cardiology, Yongin Severance Hospital, Yonsei University College of Medicine, Gyeonggi-do, South Korea.
Choongki KimDepartment of Cardiology, Ewha Womans University College of Medicine, Seoul Hospital, Seoul, South Korea.
Jaewon OhDivision of Cardiology, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Chan Joo LeeDivision of Cardiology, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Yong-Ho LeeDivision of Endocrinology and Metabolism, Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea.
Seil ParkCardiovascular Product Evaluation Center, Yonsei University College of Medicine, Seoul, South Korea.
Ok-Hee JeonCardiovascular Product Evaluation Center, Yonsei University College of Medicine, Seoul, South Korea.
Donghoon ChoiDivision of Cardiology, Yongin Severance Hospital, Yonsei University College of Medicine, Gyeonggi-do, South Korea.
Geu-Ru HongDivision of Cardiology, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. GRHONG@yuhs.ac.
Jung-Sun KimDivision of Cardiology, Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. KJS1218@yuhs.ac.ORCID 0000-0003-2263-3274
Yonsei University · KREwha Womans University · KRSamsung Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent studies have reported improved diastolic function in patients administered sodium-glucose cotransporter 2 inhibitors (SGLT2i). We aimed to investigate the effect of dapagliflozin on left ventricular (LV) diastolic function in a diabetic animal model and to determine the molecular and cellular mechanisms underlying its function.

methodsA total of 30 male New Zealand white rabbits were randomized into control, diabetes, or diabetes+dapagliflozin groups (n = 10/per each group). Diabetes was induced by intravenous alloxan. Cardiac function was evaluated using echocardiography. Myocardial samples were obtained for histologic and molecular evaluation. For cellular evaluation, fibrosis-induced cardiomyoblast (H9C2) cells were obtained, and transfection was performed for mechanism analysis (serum and glucocorticoid-regulated kinase 1 (SGK1) signaling analysis).

resultsThe diabetes+dapagliflozin group showed attenuation of diastolic dysfunction compared with the diabetes group. Dapagliflozin inhibited myocardial fibrosis via inhibition of SGK1 and epithelial sodium channel (ENaC) protein, which was observed both in myocardial tissue and H9C2 cells. In addition, dapagliflozin showed an anti-inflammatory effect and ameliorated mitochondrial disruption. Inhibition of SGK1 expression by siRNA decreased and ENaC and Na+/H+ exchanger isoform 1 (NHE1) expression was confirmed as significantly reduced as siSGK1 in the diabetes+dapagliflozin group.

conclusionsDapagliflozin attenuated left ventricular diastolic dysfunction and cardiac fibrosis via regulation of SGK1 signaling. Dapagliflozin also reduced macrophages and inflammatory proteins and ameliorated mitochondrial disruption.

Indexed as

Diabetes MellitusSodium-Glucose Transporter 2 InhibitorsAnimalsBenzhydryl CompoundsFibrosisGlucosidesMaleRabbitsBenzhydryl CompoundsdapagliflozinGlucosidesSodium-Glucose Transporter 2 InhibitorsDiabetes mellitusHeart failureLeft ventricular diastolic functionSodium-glucose cotransporter 2 inhibitor

Identifiers

PMID36068525
PMCPMC9450279
OpenAlexW4294919930

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.