Evidence map›Paper›PMID 41053180›Full record

ArticleScientific reports2025

Anti-inflammatory myeloid angiogenic cells (MIL4-MACs) attenuate angiotensin II‒induced heart failure in mice.

Toshie Kanayasu-Toyoda, Takeshi Tanaka, Kenji Yoshihara, Goki Matsumura, Katsuhiko Hayashi, Hanayuki Okura, Akifumi Matsuyama, Eriko Uchida, Teruhide Yamaguchi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Toshie Kanayasu-ToyodaDepartment of Pharmacology, Nihon Pharmaceutical University, Komuro 10,281, Inamachi, Kitaadachigun, Saitama, 362-0806, Japan.
Takeshi TanakaDepartment of Medical Safety, Tokyo Women's Medical University, Tokyo, 162-8666, Japan.
Kenji YoshiharaDepartment of Medical Safety, Tokyo Women's Medical University, Tokyo, 162-8666, Japan.
Goki MatsumuraDepartment of Medical Safety, Tokyo Women's Medical University, Tokyo, 162-8666, Japan.
Katsuhiko HayashiDivision of Microbiology, National Institute of Health Sciences, Kanagawa, 210-9501, Japan.
Hanayuki OkuraInstitute of Innovative Medical Technology, Osaka, 541-0048, Japan.
Akifumi MatsuyamaInstitute of Innovative Medical Technology, Osaka, 541-0048, Japan.
Eriko UchidaDivision of Molecular Target and Gene Therapy Products, National Institute of Health Sciences, Kanagawa, 210-9501, Japan.
Teruhide YamaguchiDepartment of Pharmacology, Nihon Pharmaceutical University, Komuro 10,281, Inamachi, Kitaadachigun, Saitama, 362-0806, Japan. t-yamaguchi@nichiyaku.ac.jp.

Funding

Japan Agency for Medical Research and Development jp20bm0404031 and JP24mk0121260
6 · The paper itself

Abstract

For cell therapy to treat heart failure, therapeutic cells should possess the abilities to promote vascularization, remodel tissues, and reduce inflammation. Previously we clarified that CD14

Indexed as

Angiotensin IIHeart FailureMyeloid CellsNeovascularization, PhysiologicAnimalsCytokinesDisease Models, AnimalHumansInflammationLipopolysaccharide ReceptorsMaleMatrix Metalloproteinase 9MiceMice, Inbred C57BLAngiotensin IICytokinesLipopolysaccharide ReceptorsMatrix Metalloproteinase 9AngiogenesisCell therapyEndothelial progenitor cellsHeart failureMacrophageMatrix metalloproteinase-9

Identifiers

PMID41053180
PMCPMC12501379

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.