Evidence mapPaperPMID 38892134Full record

ArticleInternational journal of molecular sciences2024

DNA Aptamer Raised against Advanced Glycation End Products Improves Sperm Concentration, Motility, and Viability by Suppressing Receptors for Advanced Glycation End Product-Induced Oxidative Stress and Inflammation in the Testes of Diabetic Mice.

Yusaku Mori, Michishige Terasaki, Naoya Osaka, Tomoki Fujikawa, Hironori Yashima, Tomomi Saito, Yurie Kataoka, Makoto Ohara, Yuichiro Higashimoto, Takanori Matsui and 1 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. 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
field-weighted citation impact
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.

  1. Article
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  3. Review
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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.

Yusaku MoriDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Anti-Glycation Research Section, Showa University Graduate School of Medicine, Shinagawa 142-8555, Tokyo, Japan.ORCID 0000-0002-1734-0605
Michishige TerasakiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University Graduate School of Medicine, Shinagawa 142-8555, Tokyo, Japan.ORCID 0000-0002-7405-7419
Naoya OsakaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University Graduate School of Medicine, Shinagawa 142-8555, Tokyo, Japan.
Tomoki FujikawaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University Graduate School of Medicine, Shinagawa 142-8555, Tokyo, Japan.
Hironori YashimaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University Graduate School of Medicine, Shinagawa 142-8555, Tokyo, Japan.
Tomomi SaitoDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University Graduate School of Medicine, Shinagawa 142-8555, Tokyo, Japan.
Yurie KataokaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University Graduate School of Medicine, Shinagawa 142-8555, Tokyo, Japan.
Makoto OharaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University Graduate School of Medicine, Shinagawa 142-8555, Tokyo, Japan.
Yuichiro HigashimotoDepartment of Chemistry, Kurume University School of Medicine, Kurume 830-0011, Fukuoka, Japan.ORCID 0000-0003-1382-8598
Takanori MatsuiDepartment of Bioscience and Biotechnology, Fukui Prefectural University, Eiheiji 910-1195, Fukui, Japan.ORCID 0000-0001-9506-7571
Sho-Ichi YamagishiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University Graduate School of Medicine, Shinagawa 142-8555, Tokyo, Japan.ORCID 0000-0003-0102-0823

Funding

Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan 22K15031Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology of Japan 24K12518Japan Association for Diabetes Education and Care Grants for young researchersJapanese Society of Anti-Aing Medicine Research Grant Award 2021
6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) is a risk factor for male infertility, but the underlying molecular mechanisms remain unclear. Advanced glycation end products (AGEs) are pathogenic molecules for diabetic vascular complications. Here, we investigated the effects of the DNA aptamer raised against AGEs (AGE-Apt) on testicular and sperm abnormalities in a T2DM mouse model. KK-Ay (DM) and wild-type (non-DM) 4- and 7-week-old male mice were sacrificed to collect the testes and spermatozoa for immunofluorescence, RT-PCR, and histological analyses. DM and non-DM 7-week-old mice were subcutaneously infused with the AGE-Apt or control-aptamer for 6 weeks and were then sacrificed. Plasma glucose, testicular AGEs, and

Indexed as

Aptamers, NucleotideDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Glycation End Products, AdvancedInflammationOxidative StressReceptor for Advanced Glycation End ProductsSperm MotilityTestisAnimalsMaleMiceSpermatozoaSperm CountAptamers, NucleotideGlycation End Products, AdvancedReceptor for Advanced Glycation End ProductsAGEsdiabetesDNA aptamermale infertilitysperm abnormalitytestis

Identifiers

PMID38892134
PMCPMC11172898

What Socratic holds

Textmetadata
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 Socratic graph.