Evidence map›Paper›PMID 33291667›Full record

ArticleInternational journal of molecular sciences2020

AGE-RAGE Axis Stimulates Oxidized LDL Uptake into Macrophages through Cyclin-Dependent Kinase 5-CD36 Pathway via Oxidative Stress Generation.

Hironori Yashima, Michishige Terasaki, Ami Sotokawauchi, Takanori Matsui, Yusaku Mori, Tomomi Saito, Naoya Osaka, Hideki Kushima, Munenori Hiromura, Makoto Ohara and 2 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

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  13. NWorld journal of diabetes · 2023
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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

12 authors.

Hironori YashimaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.ORCID 0000-0001-6234-8692
Michishige TerasakiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.ORCID 0000-0002-7405-7419
Ami SotokawauchiDepartment of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume 830-0011, Japan.ORCID 0000-0002-4608-9341
Takanori MatsuiDepartment of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume 830-0011, Japan.
Yusaku MoriAnti-Glycation Research Section, Department of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Tomomi SaitoDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.ORCID 0000-0002-1734-0605
Naoya OsakaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Hideki KushimaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Munenori HiromuraDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Makoto OharaDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.
Tomoyasu FukuiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.ORCID 0000-0002-8535-008X
Sho-Ichi YamagishiDepartment of Medicine, Division of Diabetes, Metabolism, and Endocrinology, Showa University School of Medicine, Tokyo 142-8666, Japan.ORCID 0000-0003-0102-0823

Funding

JSPS KAKENHI 20K06475JSPS KAKENHI 20K07075
6 · The paper itself

Abstract

Advanced glycation end products (AGEs) are localized in macrophage-derived foam cells within atherosclerotic lesions, which could be associated with the increased risk of atherosclerotic cardiovascular disease under diabetic conditions. Although foam cell formation of macrophages has been shown to be enhanced by AGEs, the underlying molecular mechanism remains unclear. Since cyclin-dependent kinase 5 (Cdk5) is reported to modulate inflammatory responses in macrophages, we investigated whether Cdk5 could be involved in AGE-induced

Indexed as

Oxidative StressAnimalsAptamers, NucleotideCD36 AntigensCyclin-Dependent Kinase 5Glycation End Products, AdvancedHumansLipoproteins, LDLMacrophagesModels, BiologicalReceptor for Advanced Glycation End ProductsU937 CellsAptamers, NucleotideCD36 AntigensCyclin-Dependent Kinase 5Glycation End Products, AdvancedLipoproteins, LDLoxidized low density lipoproteinReceptor for Advanced Glycation End ProductsAGEsCD36Cdk5macrophagesRAGE-aptamer

Identifiers

PMID33291667
PMCPMC7730944

What OpenQuestion 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 OpenQuestion graph.