Evidence map›Paper›PMID 37047475›Full record

ArticleInternational journal of molecular sciences2023

SMTP-44D Inhibits Atherosclerotic Plaque Formation in Apolipoprotein-E Null Mice Partly by Suppressing the AGEs-RAGE Axis.

Michishige Terasaki, Keita Shibata, Yusaku Mori, Tomomi Saito, Takanori Matsui, Makoto Ohara, Tomoyasu Fukui, Keiji Hasumi, Yuichiro Higashimoto, Koji Nobe and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. 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
2.5field-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

5 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  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 3 institutions in 1 country.

Michishige TerasakiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.ORCID 0000-0002-7405-7419
Keita ShibataDivision of Pharmacology, Department of Pharmacology, Toxicology and Therapeutics, School of Pharmacy, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.ORCID 0000-0002-3935-8742
Yusaku MoriDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Anti-Glycation Research Section, Showa University School of Medicine, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.ORCID 0000-0002-1734-0605
Tomomi SaitoDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.
Takanori MatsuiDepartment of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume 830-0011, Japan.ORCID 0000-0001-9506-7571
Makoto OharaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.
Tomoyasu FukuiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.
Keiji HasumiTMS Co., Ltd., KeioFuchu1chome Bldg. 11F, 1-9 Fuchucho, Fuchu-shi, Tokyo 183-0055, Japan.ORCID 0000-0002-3340-7312
Yuichiro HigashimotoDepartment of Chemistry, Kurume University School of Medicine, Kurume 830-0011, Japan.ORCID 0000-0003-1382-8598
Koji NobeDivision of Pharmacology, Department of Pharmacology, Toxicology and Therapeutics, School of Pharmacy, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
Sho-Ichi YamagishiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, 1-5-8 Shinagawa, Tokyo 142-8666, Japan.ORCID 0000-0003-0102-0823
Showa University · JPKurume University · JPTokyo University of Agriculture and Technology · JP

Funding

Japan Association for Diabetes Education and Care 2021-YNG-002Japan Society for the Promotion of Science 20K07075, 22K08318
6 · The paper itself

Abstract

SMTP-44D has been reported to have anti-oxidative and anti-inflammatory reactions, including reduced expression of receptor for advanced glycation end products (RAGE) in experimental diabetic neuropathy. Although activation of RAGE with its ligands, and advanced glycation end products (AGEs), play a crucial role in atherosclerotic cardiovascular disease, a leading cause of death in diabetic patients, it remains unclear whether SMTP-44D could inhibit experimental atherosclerosis by suppressing the AGEs-RAGE axis. In this study, we investigated the effects of SMTP-44D on atherosclerotic plaque formation and expression of AGEs in apolipoprotein-E null (

Indexed as

AtherosclerosisPlaque, AtheroscleroticAnimalsApolipoproteinsApolipoproteins EGlycation End Products, AdvancedLipoproteins, LDLMiceMice, KnockoutReceptor for Advanced Glycation End ProductsApolipoproteinsApolipoproteins EGlycation End Products, AdvancedLipoproteins, LDLReceptor for Advanced Glycation End ProductsAGEsatherosclerosisCD36Cdk5macrophagesRAGESMTP-44D

Identifiers

PMID37047475
PMCPMC10094964
OpenAlexW4362519635

What Socratic 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 Socratic graph.