Evidence map›Paper›PMID 20444914›Full record

Trial reportThe Journal of clinical endocrinology and metabolism2010

Inhibition of protein kinase Cbeta does not improve endothelial function in type 2 diabetes.

Joshua A Beckman, Allison B Goldfine, Alison Goldin, Adnan Prsic, Sora Kim, Mark A Creager

Open access · bronzeAbstract readRandomized Controlled Trial
In one paragraph

Trial report in The Journal of clinical endocrinology and metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Flow signaling and atherosclerosis.Cellular and molecular life sciences : CMLS · 2017
    Review
  5. Kinase-SUMO networks in diabetes-mediated cardiovascular disease.Metabolism: clinical and experimental · 2016
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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 at 2 institutions in 1 country.

Joshua A BeckmanBrigham and Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115, USA. jbeckman@partners.org
Allison B Goldfine
Alison Goldin
Adnan Prsic
Sora Kim
Mark A Creager
Brigham and Women's Hospital · USJoslin Diabetes Center · US

Funding

Tissue AnalysesP01HL048743 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 1992 to 2014
$26.3M
MECHANISMS OF ENDOTHELIAL DYSFUNCTION IN DIABETICSK23HL004169 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI BECKMAN, JOSHUA A · 1999 to 2003
$500k
NHLBI NIH HHS K23 HL004169NHLBI NIH HHS K23 HL-04169NHLBI NIH HHS P01 HL048743NHLBI NIH HHS P01 HL48743
6 · The paper itself

Abstract

contextAntagonism of protein kinase Cbeta (PKCbeta) restores endothelial function in experimental models of diabetes and prevents vascular dysfunction in response to hyperglycemia in healthy humans.

objectiveWe tested the hypothesis that PKCbeta antagonism would improve vascular function in subjects with type 2 diabetes compared with healthy control subjects.

designThe effect of PKCbeta was evaluated in a randomized, placebo-controlled, double-blinded crossover trial.

settingThe study was performed in the outpatient setting of a university medical center.

participantsThirteen subjects with type 2 diabetes without evidence of cardiovascular disease and 15 healthy control subjects were recruited via newspaper advertisement.

interventionSubjects underwent a randomized, double-blind, crossover, placebo-controlled trial of the selective PKCbeta antagonist ruboxistaurin mesylate. Subjects received each treatment for 14 d.

main outcome measureEndothelium-dependent and endothelium-independent vasodilation of forearm resistance vessels was measured with mercury-in-silastic, strain-gauge plethysmography during intraarterial administration of methacholine chloride and verapamil, respectively. Markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress were measured after each treatment.

resultsEndothelium-dependent vasodilation of forearm resistance vessels was attenuated in diabetic subjects when compared with healthy subjects (P=0.001). Endothelium-independent vasodilation did not differ between groups (P value not significant). Ruboxistaurin did not significantly change endothelium-dependent or endothelium-independent vasodilation or blood-based markers of inflammation, fibrinolysis, endothelial damage, and oxidative stress in either diabetic or healthy subjects.

conclusionEndothelial dysfunction of forearm resistance vessels was not improved by 2 wk of selective PKCbeta inhibition in patients with diabetes. These results suggest that PKCbeta does not contribute significantly to vascular dysfunction in otherwise healthy patients with type 2 diabetes.

Indexed as

AdultAgedAnalysis of VarianceCross-Over StudiesDiabetes Mellitus, Type 2Double-Blind MethodEndothelium, VascularEnzyme InhibitorsFemaleForearmHumansIndolesMaleMaleimidesMiddle AgedOxidative StressEnzyme InhibitorsIndolesMaleimidesProtein Kinase CProtein Kinase C betaruboxistaurin

Identifiers

PMID20444914
PMCPMC2913029
OpenAlexW2102081794

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.