Evidence map›Paper›PMID 22189563›Full record

ReviewBasic research in cardiology2012

The link between metabolic abnormalities and endothelial dysfunction in type 2 diabetes: an update.

Hanrui Zhang, Kevin C Dellsperger, Cuihua Zhang

Abstract readReview
In one paragraph

Review in Basic research in cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
7.4field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 137 citations in OpenAlex.

  1. Pooled it
  2. Correlations Between Abnormal Glucose Metabolism and Bone Mineral Density or Bone Metabolism.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Pooled it
  3. Trial
  4. Pioglitazone ameliorates endothelial dysfunction in those with impaired glucose regulation among the first-degree relatives of type 2 diabetes mellitus patients.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2013
    Trial
  5. Article
  6. Article
  7. Article
  8. Article
  9. Endothelial Metabolic Reprogramming Links Diabetes to Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Endoplasmic Reticulum Stress and Obesity.Advances in experimental medicine and biology · 2024
    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

3 authors at 1 institution in 1 country.

Hanrui ZhangDepartments of Internal Medicine, Medical Pharmacology & Physiology and Nutritional Sciences, Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO 65211, USA. hzrg7@mail.missouri.edu
Kevin C Dellsperger
Cuihua Zhang
University of Missouri · US

Funding

Role of Cytokine-Induced Inflammation in Endothelial Dysfunction in DiabetesR01HL085119 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI HILL, MICHAEL A · 2007 to 2015
$3.1M
Mechanisms of Reperfusion-induced Endothelial InjuryR01HL077566 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI HILL, MICHAEL A · 2006 to 2010
$1.8M
NHLBI NIH HHS R01 HL077566NHLBI NIH HHS R01-HL077566NHLBI NIH HHS R01 HL085119NHLBI NIH HHS R01-HL085119
6 · The paper itself

Abstract

Despite abundant clinical evidence linking metabolic abnormalities to diabetic vasculopathy, the molecular basis of individual susceptibility to diabetic vascular complications is still largely undetermined. Endothelial dysfunction in diabetes-associated vascular complications is considered an early stage of vasculopathy and has attracted considerable research interests. Type 2 diabetes is characterized by metabolic abnormalities, such as hyperglycemia, excess liberation of free fatty acids (FFA), insulin resistance and hyperinsulinemia. These abnormalities exert pathological impact on endothelial function by attenuating endothelium-mediated vasomotor function, enhancing endothelial apoptosis, stimulating endothelium activation/endothelium-monocyte adhesion, promoting an atherogenic response and suppressing barrier function. There are multiple signaling pathways contributing to the adverse effects of glucotoxicity on endothelial function. Insulin maintains the normal balance for release of several factors with vasoactive properties. Abnormal insulin signaling in the endothelium does not affect the whole-body glucose metabolism, but impairs endothelial response to insulin and accelerates atherosclerosis. Excessive level of FFA is implicated in the pathogenesis of insulin resistance. FFA induces endothelial oxidative stress, apoptosis and inflammatory response, and inhibits insulin signaling. Although hyperglycemia, insulin resistance, hyperinsulinemia and dyslipidemia independently contribute to endothelial dysfunction via various distinct mechanisms, the mutual interactions may synergistically accelerate their adverse effects. Oxidative stress and inflammation are predicted to be among the first alterations which may trigger other downstream mediators in diabetes associated with endothelial dysfunction. These mechanisms may provide insights into potential therapeutic targets that can delay or reverse diabetic vasculopathy.

Indexed as

AnimalsDiabetes Mellitus, Type 2Endothelium, VascularFatty Acids, NonesterifiedHumansHyperglycemiaInsulin ResistanceVasomotor SystemFatty Acids, Nonesterified

Identifiers

PMID22189563
PMCPMC5512574
OpenAlexW2019514289

What OpenQuestion holds

Textmetadata
LicenceTDM
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.