Evidence mapPaperPMID 35510669Full record

ArticleThe Journal of international medical research2022

Luseogliflozin inhibits high glucose-induced TGF-

Naoya Osaka, Yusaku Mori, Michishige Terasaki, Munenori Hiromura, Tomomi Saito, Hironori Yashima, Yoshie Shiraga, Raichi Kawakami, Makoto Ohara, Tomoyasu Fukui and 1 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of international medical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

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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

11 authors at 1 institution in 1 country.

Naoya OsakaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Yusaku MoriDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Anti-glycation Research Section, Showa University School of Medicine, Shinagawa, Tokyo, Japan.ORCID https://orcid.org/0000-0002-1734-0605
Michishige TerasakiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Munenori HiromuraDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Tomomi SaitoDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Hironori YashimaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Yoshie ShiragaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Raichi KawakamiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Makoto OharaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Tomoyasu FukuiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Sho-Ichi YamagishiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Shinagawa, Tokyo, Japan.
Showa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSodium-glucose cotransporter-2 (SGLT2) inhibitors exhibit cardioprotective properties in patients with diabetes. However, SGLT2 is not expressed in the heart, and the underlying molecular mechanisms are not fully understood. We investigated whether the SGLT2 inhibitor luseogliflozin exerts beneficial effects on high glucose-exposed cardiomyocytes via the suppression of sodium-hydrogen exchanger-1 (NHE-1) activity.

methodsMouse cardiomyocytes were incubated under normal or high glucose conditions with vehicle, luseogliflozin, or the NHE-1 inhibitor cariporide. NHE-1 activity and gene expression were evaluated by the SNARF assay and real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis, respectively. Six-week-old male db/db mice were treated with vehicle or luseogliflozin for 6 weeks, and the hearts were collected for histological, RT-PCR, and western blot analyses.

resultsHigh glucose increased NHE-1 activity and transforming growth factor

conclusionsLuseogliflozin may suppress cardiac hypertrophy in diabetes by reducing

Indexed as

Diabetes MellitusMyocytes, CardiacAnimalsCardiomegalyGlucoseHumansMaleMiceRNA, MessengerSodium-Glucose Transporter 2Sodium-Hydrogen Exchanger 1SorbitolTransforming Growth Factor beta21,5-anhydro-1-(5-(4-ethoxybenzyl)-2-methoxy-4-methylphenyl)-1-thioglucitolGlucoseRNA, MessengerSlc9a1 protein, mouseSodium-Glucose Transporter 2Sodium-Hydrogen Exchanger 1SorbitolTransforming Growth Factor beta2Cariporidediabetic cardiomyopathyfibrosisluseogliflozinsodium-glucose cotransporter-2 inhibitorsodium-hydrogen exchanger-1transforming growth factor-β2

Identifiers

PMID35510669
PMCPMC9082751
OpenAlexW4229076822

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.