Evidence map›Paper›PMID 31057401›Full record

ArticleFrontiers in pharmacology2019

Canagliflozin Inhibits Human Endothelial Cell Proliferation and Tube Formation.

Ghazaleh Behnammanesh, Zane E Durante, Kelly J Peyton, Luis A Martinez-Lemus, Scott M Brown, Shawn B Bender, William Durante

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.2field-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

37 citing papers in PubMed, 63 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

7 authors at 2 institutions in 1 country.

Ghazaleh BehnammaneshDepartment of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, MO, United States.
Zane E DuranteDepartment of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, MO, United States.
Kelly J PeytonDepartment of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, MO, United States.
Luis A Martinez-LemusDepartment of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, MO, United States.
Scott M BrownResearch Service, Harry S. Truman Memorial Veterans Hospital, Columbia, MO, United States.
Shawn B BenderDalton Cardiovascular Research Center, University of Missouri, Columbia, MO, United States.
William DuranteDepartment of Medical Pharmacology and Physiology, School of Medicine, University of Missouri, Columbia, MO, United States.
University of Missouri · USHarry S. Truman Memorial Veterans' Hospital · US

Funding

Mechanisms of Microvascular Remodeling ProgressionR01HL088105 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI MARTINEZ-LEMUS, LUIS A · 2009 to 2019
$3.3M
Mineralocorticoid receptor-dependent coronary vascular dysfunction in obesityR01HL136386 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI BENDER, SHAWN BRADY · 2018 to 2022
$2.8M
Mineralocorticoid Receptor-Mediated Vascular Insulin ResistanceIK2BX002030 · VA · HARRY S. TRUMAN MEMORIAL VA HOSPITAL · PI BENDER, SHAWN BRADY · 2013 to 2017
–
BLRD VA IK2 BX002030NHLBI NIH HHS R01 HL088105NHLBI NIH HHS R01 HL136386
6 · The paper itself

Abstract

Recent clinical trials revealed that sodium-glucose co-transporter 2 (SGLT2) inhibitors significantly reduce cardiovascular events in type 2 diabetic patients, however, canagliflozin increased limb amputations, an effect not seen with other SGLT2 inhibitors. Since endothelial cell (EC) dysfunction promotes diabetes-associated vascular disease and limb ischemia, we hypothesized that canagliflozin, but not other SGLT2 inhibitors, impairs EC proliferation, migration, and angiogenesis. Treatment of human umbilical vein ECs (HUVECs) with clinically relevant concentrations of canagliflozin, but not empagliflozin or dapagliflozin, inhibited cell proliferation. In particular, 10 μM canagliflozin reduced EC proliferation by approximately 45%. The inhibition of EC growth by canagliflozin occurred in the absence of cell death and was associated with diminished DNA synthesis, cell cycle arrest, and a striking decrease in cyclin A expression. Restoration of cyclin A expression

Indexed as

canagliflozinendothelial cellsmigrationproliferationtube formation

Identifiers

PMID31057401
PMCPMC6477081
OpenAlexW2938202963

What OpenQuestion holds

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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 OpenQuestion graph.