Evidence map›Paper›PMID 34413930›Full record

ArticleOxidative medicine and cellular longevity2021

DNA-Aptamer Raised against Receptor for Advanced Glycation End Products Improves Survival Rate in Septic Mice.

Yoshinori Koga, Ami Sotokawauchi, Yuichiro Higashimoto, Yuri Nishino, Naoki Hashizume, Tatsuyuki Kakuma, Jun Akiba, Yoshiaki Tanaka, Takanori Matsui, Minoru Yagi and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. 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

11 authors at 2 institutions in 1 country.

Yoshinori KogaDepartment of Pediatric Surgery, Kurume University School of Medicine, Kurume 830-0011, Japan.ORCID https://orcid.org/0000-0002-3419-8567
Ami SotokawauchiDepartment of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume 830-0011, Japan.ORCID https://orcid.org/0000-0002-4608-9341
Yuichiro HigashimotoDepartment of Chemistry, Kurume University School of Medicine, Kurume 830-0011, Japan.ORCID https://orcid.org/0000-0003-1382-8598
Yuri NishinoDepartment of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume 830-0011, Japan.
Naoki HashizumeDepartment of Pediatric Surgery, Kurume University School of Medicine, Kurume 830-0011, Japan.ORCID https://orcid.org/0000-0001-9366-361X
Tatsuyuki KakumaBiostatistics Center, Kurume University, Kurume 830-0011, Japan.ORCID https://orcid.org/0000-0002-3713-3099
Jun AkibaDepartment of Pathology, Kurume University School of Medicine, Kurume 830-0011, Japan.ORCID https://orcid.org/0000-0003-2657-8604
Yoshiaki TanakaDivision of Medical Safety Management, Kurume University Hospital, Kurume 830-0011, Japan.
Takanori MatsuiDepartment of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume 830-0011, Japan.ORCID https://orcid.org/0000-0001-9506-7571
Minoru YagiDepartment of Pediatric Surgery, Kurume University School of Medicine, Kurume 830-0011, Japan.
Sho-Ichi YamagishiDivision of Diabetes, Metabolism, and Endocrinology, Department of Medicine, Showa University School of Medicine, Tokyo 142-8666, Japan.ORCID https://orcid.org/0000-0003-0102-0823
Kurume University · JPShowa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite remarkable scientific advances in the understanding of molecular mechanisms for sepsis, therapeutic options are far from satisfactory. High mobility group box 1 (HMGB1), one of the ligands of receptor for advanced glycation end products (RAGE), is a late mediator of lethality in septic mice. We have recently found that the DNA-aptamer raised against RAGE (RAGE-aptamer) significantly blocks experimental diabetic nephropathy and melanoma growth and metastasis. We examined the effects of RAGE-aptamer on sepsis score, survival rate, and inflammatory and oxidative stress responses in serum, peripheral monocytes, kidneys and livers of lipopolysaccharide- (LPS-) injected mice, and on LPS-exposed THP-1 cells. RAGE-aptamer inhibited the binding of HMGB1 to RAGE

Indexed as

Oxidative StressAcidosisAcute Kidney InjuryAnimalsAptamers, NucleotideGlycation End Products, AdvancedHMGB1 ProteinLipopolysaccharidesLiver Failure, AcuteMaleMiceMice, Inbred BALB CNF-kappa BSepsisSurvival RateAptamers, NucleotideGlycation End Products, AdvancedHMGB1 ProteinHMGB1 protein, mouseLipopolysaccharidesNF-kappa B

Identifiers

PMID34413930
PMCPMC8369179
OpenAlexW3190637918

What OpenQuestion holds

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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.