Evidence map›Paper›PMID 34178389›Full record

ArticleImmunometabolism2021

Inflammation Meets Metabolism: Roles for the Receptor for Advanced Glycation End Products Axis in Cardiovascular Disease.

Laura Senatus, Michael MacLean, Lakshmi Arivazhagan, Lander Egaña-Gorroño, Raquel López-Díez, Michaele B Manigrasso, Henry H Ruiz, Carolina Vasquez, Robin Wilson, Alexander Shekhtman and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Immunometabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 14% 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, 19 citations in OpenAlex.

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  12. The Remnant Lipoprotein Hypothesis of Diabetes-Associated Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2022
    Review
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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

13 authors at 2 institutions in 1 country.

Laura SenatusDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Michael MacLeanDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Lakshmi ArivazhaganDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Lander Egaña-GorroñoDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Raquel López-DíezDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Michaele B ManigrassoDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Henry H RuizDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Carolina VasquezDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Robin WilsonDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Alexander ShekhtmanThe State University of New York at Albany, Albany, NY 12222, USA.
Paul F GuggerDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Ravichandran RamasamyDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
Ann Marie SchmidtDiabetes Research Program, Department of Medicine, New York University Grossman School of Medicine, New York, NY 10016, USA.
New York University · USUniversity at Albany, State University of New York · US

Funding

Resolving Macrophage Inflammation in Atherosclerotic Plaques and Other Sites in Insulin ResistanceP01HL131481 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Edward A Fisher · 2017 to 2026
$27.3M
Project 3: RAGE/DIAPH1 interactions and cellular stressP01HL146367 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SCHMIDT, ANN MARIE · 2019 to 2023
$12.5M
Training Program in Cardiovascular SciencesT32HL098129 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Glenn I Fishman, Ira J Goldberg · 2009 to 2026
$5.9M
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/mDia1, Macrophage Trafficking and Inflammation in Regression of Diabetic AtherosclerosisR01HL132516 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RAMASAMY, RAVICHANDRAN, SCHMIDT, ANN MARIE · 2017 to 2020
$2.5M
American Heart Association-American Stroke Association 17SFRN33490004NHLBI NIH HHS P01 HL131481NHLBI NIH HHS P01 HL146367NHLBI NIH HHS R01 HL132516NHLBI NIH HHS T32 HL098129NIDDK NIH HHS R01 DK109675
6 · The paper itself

Abstract

Fundamental modulation of energy metabolism in immune cells is increasingly being recognized for the ability to impart important changes in cellular properties. In homeostasis, cells of the innate immune system, such as monocytes, macrophages and dendritic cells (DCs), are enabled to respond rapidly to various forms of acute cellular and environmental stress, such as pathogens. In chronic stress milieus, these cells may undergo a re-programming, thereby triggering processes that may instigate tissue damage and failure of resolution. In settings of metabolic dysfunction, moieties such as excess sugars (glucose, fructose and sucrose) accumulate in the tissues and may form advanced glycation end products (AGEs), which are signaling ligands for the receptor for advanced glycation end products (RAGE). In addition, cellular accumulation of cholesterol species such as that occurring upon macrophage engulfment of dead/dying cells, presents these cells with a major challenge to metabolize/efflux excess cholesterol. RAGE contributes to reduced expression and activities of molecules mediating cholesterol efflux. This Review chronicles examples of the roles that sugars and cholesterol, via RAGE, play in immune cells in instigation of maladaptive cellular signaling and the mediation of chronic cellular stress. At this time, emerging roles for the ligand-RAGE axis in metabolism-mediated modulation of inflammatory signaling in immune cells are being unearthed and add to the growing body of factors underlying pathological immunometabolism.

Indexed as

cholesterol metabolismdendritic celldiabetesimmune cellinterferon signalingmonocyte/macrophagereceptor for advanced glycation end products (RAGE)sugar metabolism

Identifiers

PMID34178389
PMCPMC8232874
OpenAlexW3172158917

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.