Evidence map›Paper›PMID 32489701›Full record

ArticleAging and disease2020

Neuroprotective Effects of Endogenous Secretory Receptor for Advanced Glycation End-products in Brain Ischemia.

Yu Shimizu, Ai Harashima, Seiichi Munesue, Masahiro Oishi, Tsuyoshi Hattori, Osamu Hori, Yasuko Kitao, Hiroshi Yamamoto, Nontaphat Leerach, Mitsutoshi Nakada and 2 more

Open access · goldAbstract read
In one paragraph

Article in Aging and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. International journal of molecular sciences · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Navigating Central Oxytocin Transport: Known Realms and Uncharted Territories.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025
    Review
  7. Article
  8. Article
  9. Cells · 2023
    Article
  10. Advanced Glycation End-Products and Diabetic Neuropathy of the Retina.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Dual Nature of RAGE in Host Reaction and Nurturing the Mother-Infant Bond.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Is carbonyl/AGE/RAGE stress a hallmark of the brain aging?Pflugers Archiv : European journal of physiology · 2021
    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

12 authors at 2 institutions in 2 countries.

Yu Shimizu1Department of Biochemistry and Molecular Vascular Biology.
Ai Harashima1Department of Biochemistry and Molecular Vascular Biology.
Seiichi Munesue1Department of Biochemistry and Molecular Vascular Biology.
Masahiro Oishi1Department of Biochemistry and Molecular Vascular Biology.
Tsuyoshi Hattori3Department of Neuroanatomy, Kanazawa University Graduate School of Medical Sciences, Kanazawa 920-8641, Japan.
Osamu Hori3Department of Neuroanatomy, Kanazawa University Graduate School of Medical Sciences, Kanazawa 920-8641, Japan.
Yasuko Kitao3Department of Neuroanatomy, Kanazawa University Graduate School of Medical Sciences, Kanazawa 920-8641, Japan.
Hiroshi Yamamoto1Department of Biochemistry and Molecular Vascular Biology.
Nontaphat Leerach1Department of Biochemistry and Molecular Vascular Biology.
Mitsutoshi Nakada2Department of Neurosurgery and.
Yasuhiko Yamamoto1Department of Biochemistry and Molecular Vascular Biology.
Yasuhiko Hayashi2Department of Neurosurgery and.
Center for Vascular Biology Research · USKanazawa Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The receptor for advanced glycation end-products (RAGE) is expressed on human brain endothelial cells (HBEC) and is implicated in neuronal cell death after ischemia. We report that endogenous secretory RAGE (esRAGE) is a splicing variant form of RAGE that functions as a decoy against ischemia-induced neuronal cell damage. This study demonstrated that esRAGE was associated with heparan sulphate proteoglycans on HBEC. The parabiotic experiments between human esRAGE overexpressing transgenic (Tg), RAGE knockout (KO), and wild-type (WT) mice revealed a significant neuronal cell damage in the CA1 region of the WT side of parabiotic WT→WT mice, but not of Tg→WT mice, 7 days after bilateral common carotid artery occlusion. Human esRAGE was detected around the CA1 neurons in the WT side of the parabiotic Tg→WT pair, but not in the KO side of the Tg→KO pair. To elucidate the dynamic transfer of esRAGE into the brain, we used the blood-brain barrier (BBB) system (PharmaCo-Cell) with or without RAGE knockdown in endothelial cells. A RAGE-dependent transfer of esRAGE was demonstrated from the vascular to the brain side. These findings suggested that esRAGE is associated with heparan sulphate proteoglycans and is transferred into the brain via BBB to exert its neuroprotective effects in ischemia.

Indexed as

blood-brain barrierdelayed neuronal cell damageendogenous secretory RAGE (esRAGE)parabiosisReceptor for advanced glycation end-products (RAGE)

Identifiers

PMID32489701
PMCPMC7220285
OpenAlexW3025019874

What OpenQuestion holds

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LicenceCC BY
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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.