Evidence map›Paper›PMID 33131091›Full record

ReviewFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

The role of RAGE in host pathology and crosstalk between RAGE and TLR4 in innate immune signal transduction pathways.

Daniel Prantner, Shreeram Nallar, Stefanie N Vogel

Open access · bronzeAbstract readReview
In one paragraph

Review in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Aging-related CD8PeerJ · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Virtual Probing on the Influence of CaCell biochemistry and biophysics · 2025
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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 1 institution in 2 countries.

Daniel PrantnerDepartment of Microbiology and Immunology, School of Medicine, University of Maryland, Baltimore, MD, USA.
Shreeram NallarInstitute of Human Virology, School of Medicine, University of Maryland, Baltimore, MD, USA.
Stefanie N VogelDepartment of Microbiology and Immunology, School of Medicine, University of Maryland, Baltimore, MD, USA.
University of Maryland, Baltimore · US

Funding

Targeting TLR Signaling Pathways to Blunt Pathogen-mediated Acute Lung InjuryR01AI125215 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI BLANCO, JORGE C, VOGEL, STEFANIE N. · 2017 to 2021
$2.7M
Macrophage differentiation and disease outcome in influenza infectionR01AI123371 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2017 to 2021
$2.7M
Analysis of Cellular Metabolism using Seahhorse TechnologyS10OD025101 · OD · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2019 to 2019
$205k
NIAID NIH HHS R01 AI123371NIAID NIH HHS R01 AI125215NIH HHS S10 OD025101
6 · The paper itself

Abstract

Although the innate immune receptor protein, Receptor for Advanced Glycation End products (RAGE), has been extensively studied, there has been renewed interest in RAGE for its potential role in sepsis, along with a host of other inflammatory diseases of chronic, noninfectious origin. In contrast to other innate immune receptors, for example, Toll-like receptors (TLRs), that recognize ligands derived from pathogenic organisms that are collectively known as "pathogen-associated molecular patterns" (PAMPs) or host-derived "damage-associated molecular patterns" (DAMPs), RAGE has been shown to recognize a broad collection of DAMPs exclusively. Historically, these DAMPs have been shown to be pro-inflammatory in nature. Early studies indicated that the adaptor molecule, MyD88, might be important for this change. More recent studies have explored further the mechanisms underlying this inflammatory change. Overall, the newer results have shown that there is extensive crosstalk between RAGE and TLRs. The three canonical RAGE ligands, Advanced Glycation End products (AGEs), HMGB1, and S100 proteins, have all been shown to activate both TLRs and RAGE to varying degrees in order to induce inflammation in in vitro models. As with any field that delves deeply into innate signaling, obstacles of reagent purity may be a cause of some of the discrepancies in the literature, and we have found that commercial antibodies that have been widely used exhibit a high degree of nonspecificity. Nonetheless, the weight of published evidence has led us to speculate that RAGE may be physically interacting with TLRs on the cell surface to elicit inflammation via MyD88-dependent signaling.

Indexed as

AnimalsHumansImmunity, InnateInflammationReceptor for Advanced Glycation End ProductsSignal TransductionToll-Like Receptor 4Receptor for Advanced Glycation End ProductsToll-Like Receptor 4DAMPsHMGB1inflammationtoll-like receptors

Identifiers

PMID33131091
PMCPMC8121140
OpenAlexW3096351980

What Socratic 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 Socratic graph.