Evidence map›Paper›PMID 35956875›Full record

ReviewMolecules (Basel, Switzerland)2022

Receptor for Advanced Glycation End Products (RAGE): A Pivotal Hub in Immune Diseases.

Qing Yue, Yu Song, Zi Liu, Lin Zhang, Ling Yang, Jinlong Li

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
10.5field-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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 87 citations in OpenAlex.

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9 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 2 institutions in 1 country.

Qing YueHebei Key Laboratory for Organ Fibrosis Research, School of Public Health, North China University of Science and Technology, Tangshan 063210, China.ORCID 0000-0002-5456-8772
Yu SongHebei Key Laboratory for Organ Fibrosis Research, School of Public Health, North China University of Science and Technology, Tangshan 063210, China.ORCID 0000-0003-1403-4183
Zi LiuHebei Key Laboratory for Organ Fibrosis Research, School of Public Health, North China University of Science and Technology, Tangshan 063210, China.ORCID 0000-0002-6445-1033
Lin ZhangDepartment of Internal Medicine Nursing, School of Nursing, Wannan Medical College, 22 Wenchang West Road, Higher Education Park, Wuhu 241002, China.
Ling YangHebei Key Laboratory for Organ Fibrosis Research, School of Public Health, North China University of Science and Technology, Tangshan 063210, China.ORCID 0000-0002-9103-3494
Jinlong LiHebei Key Laboratory for Organ Fibrosis Research, School of Public Health, North China University of Science and Technology, Tangshan 063210, China.ORCID 0000-0002-5332-6659
North China University of Science and Technology · CNWannan Medical College · CN

Funding

Basic Research Program of Science and Technology in the Education Department of Hebei Province JQN2019012National Natural Science Foundation of China No. 82003404Natural Science Foundation of Hebei Province H2019209576
6 · The paper itself

Abstract

As a critical molecule in the onset and sustainment of inflammatory response, the receptor for advanced glycation end products (RAGE) has a variety of ligands, such as advanced glycation end products (AGEs), S100/calcium granule protein, and high-mobility group protein 1 (HMGB1). Recently, an increasing number studies have shown that RAGE ligand binding can initiate the intracellular signal cascade, affect intracellular signal transduction, stimulate the release of cytokines, and play a vital role in the occurrence and development of immune-related diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and Alzheimer's disease. In addition, other RAGE signaling pathways can play crucial roles in life activities, such as inflammation, apoptosis, autophagy, and endoplasmic reticulum stress. Therefore, the strategy of targeted intervention in the RAGE signaling pathway may have significant therapeutic potential, attracting increasing attention. In this paper, through the systematic induction and analysis of RAGE-related signaling pathways and their regulatory mechanisms in immune-related diseases, we provide theoretical clues for the follow-up targeted intervention of RAGE-mediated diseases.

Indexed as

Glycation End Products, AdvancedImmune System DiseasesReceptor for Advanced Glycation End ProductsHumansInflammationS100 ProteinsSignal TransductionGlycation End Products, AdvancedReceptor for Advanced Glycation End ProductsS100 Proteinsadvanced glycation end-product receptorhigh-mobility group protein 1immunenuclear factor kappa-B

Identifiers

PMID35956875
PMCPMC9370360
OpenAlexW4289519993

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.