Evidence map›Paper›PMID 27967251›Full record

ReviewExpert review of proteomics2017

Glycation & the RAGE axis: targeting signal transduction through DIAPH1.

Alexander Shekhtman, Ravichandran Ramasamy, Ann Marie Schmidt

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Expert review of proteomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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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 2 institutions in 1 country.

Alexander Shekhtmana Department of Chemistry , University at Albany, State University of New York , Albany , NY , 12222 , USA.
Ravichandran Ramasamyb Diabetes Research Program, Division of Endocrinology, Department of Medicine , NYU Langone Medical Center , New York , NY , 10016 , USA.
Ann Marie Schmidtb Diabetes Research Program, Division of Endocrinology, Department of Medicine , NYU Langone Medical Center , New York , NY , 10016 , USA.
NYU Langone Health · USAlbany State University · US

Funding

VASCULAR AND MONOCYTE DYSFUNCTION IN WOUND REPAIRP01HL060901 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI YAN, SHI FANG · 1999 to 2017
$20.2M
Targeting RAGE-mDia1 in Diabetic Complications: Mechanisms and TherapeuticsR24DK103032 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RAMASAMY, RAVICHANDRAN, SCHMIDT, ANN MARIE · 2014 to 2018
$4.2M
RAGE/mDia1, Macrophage Trafficking and Inflammation in High Fat FeedingR01DK109675 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RAMASAMY, RAVICHANDRAN, SCHMIDT, ANN MARIE · 2016 to 2020
$2.6M
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 HL118565NIDDK NIH HHS R01 DK109675NIDDK NIH HHS R24 DK103032
6 · The paper itself

Abstract

introductionThe consequences of chronic disease are vast and unremitting; hence, understanding the pathogenic mechanisms mediating such disorders holds promise to identify therapeutics and diminish the consequences. The ligands of the receptor for advanced glycation end products (RAGE) accumulate in chronic diseases, particularly those characterized by inflammation and metabolic dysfunction. Although first discovered and reported as a receptor for advanced glycation end products (AGEs), the expansion of the repertoire of RAGE ligands implicates the receptor in diverse milieus, such as autoimmunity, chronic inflammation, obesity, diabetes, and neurodegeneration. Areas covered: This review summarizes current knowledge regarding the ligand families of RAGE and data from human subjects and animal models on the role of the RAGE axis in chronic diseases. The recent discovery that the cytoplasmic domain of RAGE binds to the formin homology 1 (FH1) domain, DIAPH1, and that this interaction is essential for RAGE ligand-stimulated signal transduction, is discussed. Finally, we review therapeutic opportunities targeting the RAGE axis as a means to mitigate chronic diseases. Expert commentary: With the aging of the population and the epidemic of cardiometabolic disease, therapeutic strategies to target molecular pathways that contribute to the sequelae of these chronic diseases are urgently needed. In this review, we propose that the ligand/RAGE axis and its signaling nexus is a key factor in the pathogenesis of chronic disease and that therapeutic interruption of this pathway may improve quality and duration of life.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntigens, NeoplasmDiabetes ComplicationsDisease Models, AnimalForminsGlycation End Products, AdvancedHumansMitogen-Activated Protein KinasesNeurodegenerative DiseasesObesityReceptor for Advanced Glycation End ProductsSignal TransductionAdaptor Proteins, Signal TransducingAger protein, mouseAntigens, NeoplasmDIAPH1 protein, humanForminsGlycation End Products, AdvancedMitogen-Activated Protein KinasesMOK protein, humanReceptor for Advanced Glycation End ProductsdiabetesDIAPH1GlycationinflammationneurodegenerationobesityRAGEreceptor for AGE

Identifiers

PMID27967251
PMCPMC5535775
OpenAlexW2566764752

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.