Evidence map›Paper›PMID 7544803›Full record

ArticleThe Journal of clinical investigation1995

Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes.

A M Schmidt, O Hori, J X Chen, J F Li, J Crandall, J Zhang, R Cao, S D Yan, J Brett, D Stern

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 223 papers.

0numbers the graph read from it
0cells of the map it votes in
223citing papers in PubMed
22.4field-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.

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

223 citing papers in PubMed, 893 citations in OpenAlex.

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  5. HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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  14. Inflammation, diabetic foot and related treatments.Frontiers in endocrinology · 2025
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163 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

10 authors at 1 institution in 1 country.

A M SchmidtDepartment of Medicine, Columbia University-College of Physicians and Surgeons, New York, New York 10032, USA.
O Hori
J X Chen
J F Li
J Crandall
J Zhang
R Cao
S D Yan
J Brett
D Stern
Columbia University · US

Funding

VITAMIN A TRANSPORT AND RETINOL-BINDING PROTEIN METABOLISMP50HL021006 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI TALL, ALAN RICHARD · 1985 to 1996
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TUMOR-INDUCED MODULATION OF ENDOTHELIAL CELL FUNCTIONR01HL042833 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI STERN, DAVID M. · 1989 to 1998
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NHLBI NIH HHS HL-21006NHLBI NIH HHS HL-42833NIA NIH HHS AG-00602
6 · The paper itself

Abstract

Vascular cell adhesion molecule-1 (VCAM-1), an inducible cell-cell recognition protein on the endothelial cell surface (EC), has been associated with early stages of atherosclerosis. In view of the accelerated vascular disease observed in patients with diabetes, and the enhanced expression of VCAM-1 in diabetic rabbits, we examined whether irreversible advanced glycation endproducts (AGEs), could mediate VCAM-1 expression by interacting with their endothelial cell receptor (receptor for AGE, RAGE). Exposure of cultured human ECs to AGEs induced expression of VCAM-1, increased adhesivity of the monolayer for Molt-4 cells, and was associated with increased levels of VCAM-1 transcripts. The inhibitory effect of anti-RAGE IgG, a truncated form of the receptor (soluble RAGE) or N-acetylcysteine on VCAM-1 expression indicated that AGE-RAGE-induced oxidant stress was central to VCAM-1 induction. Electrophoretic mobility shift assays on nuclear extracts from AGE-treated ECs showed induction of specific DNA binding activity for NF-kB in the VCAM-1 promoter, which was blocked by anti-RAGE IgG or N-acetylcysteine. Soluble VCAM-1 antigen was elevated in human diabetic plasma. These data are consistent with the hypothesis that AGE-RAGE interaction induces expression of VCAM-1 which can prime diabetic vasculature for enhanced interaction with circulating monocytes.

Indexed as

Gene ExpressionAnimalsBase SequenceCell AdhesionCell Adhesion MoleculesCell LineCell NucleusCells, CulturedDiabetic AngiopathiesDNA PrimersEndothelium, VascularEnzyme-Linked Immunosorbent AssayGlycation End Products, AdvancedHumansMaleMiceCell Adhesion MoleculesDNA PrimersGlycation End Products, AdvancedReceptor for Advanced Glycation End ProductsReceptors, ImmunologicVascular Cell Adhesion Molecule-1

Identifiers

PMID7544803
PMCPMC185762
OpenAlexW2138928713

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.