Evidence map›Paper›PMID 24084731›Full record

ReviewInternational journal of molecular sciences2013

Radical roles for RAGE in the pathogenesis of oxidative stress in cardiovascular diseases and beyond.

Gurdip Daffu, Carmen Hurtado del Pozo, Karen M O'Shea, Radha Ananthakrishnan, Ravichandran Ramasamy, Ann Marie Schmidt

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 1 pooled it
12.1field-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

119 citing papers in PubMed, 1 synthesis or guideline pooled it, 217 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Molecules (Basel, Switzerland) · 2026
    Article
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  20. Spotlight on the Mechanism of Action of Semaglutide.Current issues in molecular biology · 2024
    Review

59 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

6 authors at 1 institution in 1 country.

Gurdip DaffuDiabetes Research Program, Division of Endocrinology, Department of Medicine, New York University Langone Medical Center, 550 First Avenue, Smilow 901C, New York, NY 10016, USA. annmarie.schmidt@nyumc.org.
Carmen Hurtado del Pozo
Karen M O'Shea
Radha Ananthakrishnan
Ravichandran Ramasamy
Ann Marie Schmidt
NYU Langone Health · US

Funding

VASCULAR AND MONOCYTE DYSFUNCTION IN WOUND REPAIRP01HL060901 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RAMASAMY, RAVICHANDRAN, SCHMIDT, ANN MARIE · 1999 to 2017
$20.2M
RAGE, Macrophages & HDL BiologyR01HL118565 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SCHMIDT, ANN MARIE · 2013 to 2017
$2.1M
NHLBI NIH HHS P01 HL060901NHLBI NIH HHS R01 HL118565
6 · The paper itself

Abstract

Oxidative stress is a central mechanism by which the receptor for advanced glycation endproducts (RAGE) mediates its pathological effects. Multiple experimental inquiries in RAGE-expressing cultured cells have demonstrated that ligand-RAGE interaction mediates generation of reactive oxygen species (ROS) and consequent downstream signal transduction and regulation of gene expression. The primary mechanism by which RAGE generates oxidative stress is via activation of NADPH oxidase; amplification mechanisms in the mitochondria may further drive ROS production. Recent studies indicating that the cytoplasmic domain of RAGE binds to the formin mDia1 provide further support for the critical roles of this pathway in oxidative stress; mDia1 was required for activation of rac1 and NADPH oxidase in primary murine aortic smooth muscle cells treated with RAGE ligand S100B. In vivo, in multiple distinct disease models in animals, RAGE action generates oxidative stress and modulates cellular/tissue fate in range of disorders, such as in myocardial ischemia, atherosclerosis, and aneurysm formation. Blockade or genetic deletion of RAGE was shown to be protective in these settings. Indeed, beyond cardiovascular disease, evidence is accruing in human subjects linking levels of RAGE ligands and soluble RAGE to oxidative stress in disorders such as doxorubicin toxicity, acetaminophen toxicity, neurodegeneration, hyperlipidemia, diabetes, preeclampsia, rheumatoid arthritis and pulmonary fibrosis. Blockade of RAGE signal transduction may be a key strategy for the prevention of the deleterious consequences of oxidative stress, particularly in chronic disease.

Indexed as

AnimalsCardiovascular DiseasesGlycation End Products, AdvancedHumansOxidative StressSignal TransductionGlycation End Products, Advanced

Identifiers

PMID24084731
PMCPMC3821592
OpenAlexW1999908383

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.