Evidence map›Paper›PMID 17179929›Full record

ReviewNature clinical practice. Endocrinology & metabolism2007

Mechanisms of Disease: endothelial dysfunction in insulin resistance and diabetes.

Christian Rask-Madsen, George L King

2 registry-linked trialsAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature clinical practice. Endocrinology & metabolism, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 211 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
211citing papers in PubMed, 2 pooled it
22.3field-weighted citation impact, top 1% 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.

NCT02964585 phase4completedstarted 2016, after this paper: background citation

Role of Canagliflozin on Gene Expression and Function of CD34+ Endothelial Progenitor Cells and Renal Function in Patients With Type 2 Diabetes

Ran2016Enrolled34Registered outcomes18Posted comparisons0ConditionsType 2 Diabetes MellitusArmsCanagliflozin, Placebo
Open the trial in the graph
NCT03862547 naunknown statusnot on this mapstarted 2019, after this paper: background citation

Role and Clinical Relevance of Nerve Growth Factor (NGF) and Its Receptors (TrKA and p75NTR) in Patients With Erectile Dysfunction and Diabetes With or Wothout Metabolic Syndrome

TypeinterventionalSponsorUniversity Of PerugiaRan2019 to 2020Enrolled40ConditionsErectile DysfunctionArmsA peripheral blood sample from the cubital vein
3 · Its place in the literature

Who cites it

211 citing papers in PubMed, 2 syntheses or guidelines pooled it, 474 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Trial
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

151 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Christian Rask-MadsenJoslin Diabetes Center, Harvard Medical School, Boston, MA 02120, USA.
George L King
Harvard University · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
SELECTIVE INSULIN RESISTANCE--DIABETIC VASCULAR DISEASER01DK053105 · NIDDK · JOSLIN DIABETES CENTER · PI KING, GEORGE L · 1997 to 2017
$5.0M
PKC Activation and Cardiovascular Disease in DiabetesR01DK071359 · NIDDK · JOSLIN DIABETES CENTER · PI KING, GEORGE L · 2004 to 2007
$1.8M
NIDDK NIH HHS 5 P30 DK36836NIDDK NIH HHS DK53105NIDDK NIH HHS DK71359
6 · The paper itself

Abstract

Endothelial dysfunction is one manifestation of the many changes induced in the arterial wall by the metabolic abnormalities accompanying diabetes and insulin resistance. In type 1 diabetes, endothelial dysfunction is most consistently found in advanced stages of the disease. In other patients, it is associated with nondiabetic insulin resistance and probably precedes type 2 diabetes. In obesity and insulin resistance, increased secretion of proinflammatory cytokines and decreased secretion of adiponectin from adipose tissue, increased circulating levels of free fatty acids, and postprandial hyperglycemia can all alter gene expression and cell signaling in vascular endothelium, cause vascular insulin resistance, and change the release of endothelium-derived factors. In diabetes, sustained hyperglycemia causes increased intracellular concentrations of glucose metabolites in endothelial cells. These changes cause mitochondrial dysfunction, increased oxidative stress, and activation of protein kinase C. Dysfunctional endothelium displays activation of vascular NADPH oxidase, uncoupling of endothelial nitric oxide synthase, increased expression of endothelin 1, a changed balance between the production of vasodilator and vasoconstrictor prostanoids, and induction of adhesion molecules. This review describes how these and other changes influence endothelium-dependent vasodilation in patients with insulin resistance and diabetes. The clinical utility of endothelial function testing and future therapeutic targets is also discussed.

Indexed as

Insulin ResistanceDiabetes Mellitus, Type 2Diabetic AngiopathiesEndothelial CellsEndothelium, VascularHumansModels, BiologicalVasodilation

Identifiers

PMID17179929
OpenAlexW2082502030

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.