Evidence map›Paper›PMID 18245812›Full record

ArticleThe American journal of pathology2008

A role for the receptor for advanced glycation end products in idiopathic pulmonary fibrosis.

Judson M Englert, Lana E Hanford, Naftali Kaminski, Jacob M Tobolewski, Roderick J Tan, Cheryl L Fattman, Lasse Ramsgaard, Thomas J Richards, Inna Loutaev, Peter P Nawroth and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 1 pooled it
15.7field-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

116 citing papers in PubMed, 1 synthesis or guideline pooled it, 218 citations in OpenAlex.

  1. Receptor for advanced glycation end-products and environmental exposure related obstructive airways disease: a systematic review.European respiratory review : an official journal of the European Respiratory Society · 2019
    Pooled it
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  11. Cell Proliferation and Apoptosis-Key Players in the Lung Aging Process.International journal of molecular sciences · 2024
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56 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

13 authors at 4 institutions in 2 countries.

Judson M EnglertDepartment of Pathology,University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Lana E Hanford
Naftali Kaminski
Jacob M Tobolewski
Roderick J Tan
Cheryl L Fattman
Lasse Ramsgaard
Thomas J Richards
Inna Loutaev
Peter P Nawroth
Michael Kasper
Angelika Bierhaus
Tim D Oury
University of Pittsburgh · USHeidelberg University · DETU Dresden · DEUniversity of Washington · US

Funding

New Molecular Targets in Pulmonary FibrosisR01HL073745 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAMINSKI, NAFTALI · 2003 to 2006
$2.8M
EXTRACELLULAR SUPEROXIDE DISMUTASE IN PULMONARY FIBROSISR01HL063700 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OURY, TIM D · 2000 to 2009
$2.7M
The Role of RAGE in AsbestosisR21ES013986 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OURY, TIM D · 2006 to 2007
$397k
EC-SOD in Asbestos-Induced Lung InjuryF30ES013621 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI TAN, RODERICK JASON · 2004 to 2006
$123k
NHLBI NIH HHS R01 HL063700NHLBI NIH HHS R01HL063700NHLBI NIH HHS R01 HL073745NHLBI NIH HHS R01HL073745NHLBI NIH HHS R01HL110166NIEHS NIH HHS F30 ES013621NIEHS NIH HHS F30ES013621NIEHS NIH HHS R21 ES013986NIEHS NIH HHS R21ES013986
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a severely debilitating disease associated with a dismal prognosis. There are currently no effective therapies for IPF, thus the identification of novel therapeutic targets is greatly needed. The receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily of cell surface receptors whose activation has been linked to various pathologies. In healthy adult animals, RAGE is expressed at the highest levels in the lung compared to other tissues. To investigate the hypothesis that RAGE is involved in IPF pathogenesis, we have examined its expression in two mouse models of pulmonary fibrosis and in human tissue from IPF patients. In each instance we observed a depletion of membrane RAGE and its soluble (decoy) isoform, sRAGE, in fibrotic lungs. In contrast to other diseases in which RAGE signaling promotes pathology, immunohistochemical and hydroxyproline quantification studies on aged RAGE-null mice indicate that these mice spontaneously develop pulmonary fibrosis-like alterations. Furthermore, when subjected to a model of pulmonary fibrosis, RAGE-null mice developed more severe fibrosis, as measured by hydroxyproline assay and histological scoring, than wild-type controls. Combined with data from other studies on mouse models of pulmonary fibrosis and human IPF tissues indicate that loss of RAGE contributes to IPF pathogenesis.

Indexed as

Age FactorsAnimalsAsbestosAsbestosisCattleDown-RegulationHumansLungMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutPulmonary FibrosisReceptor for Advanced Glycation End ProductsReceptors, ImmunologicAsbestosMembrane ProteinsReceptor for Advanced Glycation End ProductsReceptors, Immunologic

Identifiers

PMID18245812
PMCPMC2258251
OpenAlexW1979937536

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.