Evidence mapPaperPMID 32101837Full record

ArticleJournal of atherosclerosis and thrombosis2020

Canagliflozin Prevents Diabetes-Induced Vascular Dysfunction in ApoE-Deficient Mice.

Arief Rahadian, Daiju Fukuda, Hotimah Masdan Salim, Shusuke Yagi, Kenya Kusunose, Hirotsugu Yamada, Takeshi Soeki, Masataka Sata

Open access · diamondAbstract read
In one paragraph

Article in Journal of atherosclerosis and thrombosis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. SGLT2 Inhibitors in Aging-Related Cardiovascular Disease: A Review of Potential Mechanisms.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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

8 authors at 1 institution in 1 country.

Arief RahadianDepartment of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
Daiju FukudaDepartment of Cardio-Diabetes Medicine, Tokushima University Graduate School of Biomedical Sciences.
Hotimah Masdan SalimDepartment of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
Shusuke YagiDepartment of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
Kenya KusunoseDepartment of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
Hirotsugu YamadaDepartment of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
Takeshi SoekiDepartment of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
Masataka SataDepartment of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
Tokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimRecent studies have demonstrated that selective sodium-glucose cotransporter 2 inhibitors (SGLT2is) reduce cardiovascular events, although their mechanism remains obscure. We examined the effect of canagliflozin, an SGLT2i, on atherogenesis and investigated its underlying mechanism.

methodCanagliflozin (30 mg/kg/day) was administered by gavage to streptozotocin-induced diabetic apolipoprotein E-deficient (ApoE

resultCanagliflozin decreased blood glucose (P<0.001) and total cholesterol (P<0.05) levels. Sudan IV staining showed that 12-week canagliflozin treatment decreased atherosclerotic lesions (P<0.05). Further, 8-week canagliflozin treatment ameliorated endothelial dysfunction, as determined by acetylcholine-induced vasodilation (P<0.05), and significantly reduced the expressions of inflammatory molecules such as ICAM-1 and VCAM-1 in the aorta at the RNA and protein levels. Canagliflozin also reduced the expressions of NADPH oxidase subunits such as NOX2 and p22phox in the aorta and reduced urinary excretion of 8-OHdG, suggesting a reduction in oxidative stress. Methylglyoxal, a precursor of advanced glycation end products, increased the expressions of ICAM-1 and p22phox in HUVECs (P<0.05, both). Methylglyoxal also decreased the phosphorylation of eNOS

conclusionCanagliflozin prevents endothelial dysfunction and atherogenesis in diabetic ApoE

Indexed as

AnimalsAortaApolipoproteins EAtherosclerosisCanagliflozinDiabetes ComplicationsDiabetes Mellitus, ExperimentalEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsImmunohistochemistryInflammationIn Vitro TechniquesMaleMiceMice, Inbred C57BLApolipoproteins ECanagliflozinSodium-Glucose Transporter 2 InhibitorsAtherosclerosisCanagliflozinEndothelial dysfunctionSGLT2 inhibitor

Identifiers

PMID32101837
PMCPMC7803832
OpenAlexW3006947875

What Socratic holds

Texttitle and abstract
LicenceCC BY-NC-SA
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.