Evidence map›Paper›PMID 34812852›Full record

ArticleBiology open2022

Soluble receptor for advanced glycation end products protects from ischemia- and reperfusion-induced acute kidney injury.

Taro Miyagawa, Yasunori Iwata, Megumi Oshima, Hisayuki Ogura, Koichi Sato, Shiori Nakagawa, Yuta Yamamura, Yasutaka Kamikawa, Taito Miyake, Shinji Kitajima and 9 more

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. High-mobility group box 1 in acute kidney injury.Frontiers in pharmacology · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Dual Nature of RAGE in Host Reaction and Nurturing the Mother-Infant Bond.International journal of molecular sciences · 2022
    Review
  12. Article
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

19 authors at 2 institutions in 1 country.

Taro MiyagawaDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0003-0186-7362
Yasunori IwataDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0002-4756-5207
Megumi OshimaDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0002-4108-5229
Hisayuki OguraDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.
Koichi SatoDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.
Shiori NakagawaDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.
Yuta YamamuraDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0003-3713-0733
Yasutaka KamikawaDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0002-4819-8349
Taito MiyakeDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0002-2416-2181
Shinji KitajimaDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0002-6532-6496
Tadashi ToyamaDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0003-0162-6286
Akinori HaraDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0002-0399-1474
Norihiko SakaiDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0001-7245-9716
Miho ShimizuDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0002-7737-935X
Kengo FuruichiDepartment of Nephrology, Kanazawa Medical University School of Medicine, 1-1 Daigaku, Uchinada, Kahoku, Ishikawa 920-0293, Japan.ORCID 0000-0002-7069-0938
Seiichi MunesueDepartment of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Sciences, 13-1 Takara-machi, Kanazawa 920-8641, Japan.
Yasuhiko YamamotoDepartment of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Sciences, 13-1 Takara-machi, Kanazawa 920-8641, Japan.ORCID 0000-0003-1326-4649
Shuichi KanekoDepartment of System Biology, Institute of Medical Pharmaceutical and Health Science, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.
Takashi WadaDepartment of Nephrology and Laboratory Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-8641, Japan.
Kanazawa University · JPKanazawa Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The full-length receptor for advanced glycation end products (RAGE) is a multiligand pattern recognition receptor. High-mobility group box 1 (HMGB1) is a RAGE ligand of damage-associated molecular patterns that elicits inflammatory reactions. The shedded isoform of RAGE and endogenous secretory RAGE (esRAGE), a splice variant, are soluble isoforms (sRAGE) that act as organ-protective decoys. However, the pathophysiologic roles of RAGE/sRAGE in acute kidney injury (AKI) remain unclear. We found that AKI was more severe, with enhanced renal tubular damage, macrophage infiltration, and fibrosis, in mice lacking both RAGE and sRAGE than in wild-type (WT) control mice. Using murine tubular epithelial cells (TECs), we demonstrated that hypoxia upregulated messenger RNA (mRNA) expression of HMGB1 and tumor necrosis factor α (TNF-α), whereas RAGE and esRAGE expressions were paradoxically decreased. Moreover, the addition of recombinant sRAGE canceled hypoxia-induced inflammation and promoted cell viability in cultured TECs. sRAGE administration prevented renal tubular damage in models of ischemia/reperfusion-induced AKI and of anti-glomerular basement membrane (anti-GBM) glomerulonephritis. These results suggest that sRAGE is a novel therapeutic option for AKI.

Indexed as

Acute Kidney InjuryAnimalsIschemiaMiceProtein IsoformsReceptor for Advanced Glycation End ProductsReperfusionProtein IsoformsReceptor for Advanced Glycation End ProductsAcute kidney injuryHigh-mobility group box 1 (HMGB1)Ischemia and reperfusionReceptor for advanced glycation end products (RAGE)Soluble receptor for advanced glycation end products (sRAGE)

Identifiers

PMID34812852
PMCPMC8822355
OpenAlexW3216823806

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.