Evidence map›Paper›PMID 40490490›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2025

Transferrin receptor 1 deficiency in smooth muscle cells attenuates vascular remodeling in hypertensive mice.

Yoshiro Naito, Hisashi Sawada, Tetsuo Horimatsu, Masaki Ohmuraya, Masanori Asakura, Masaharu Ishihara

Abstract read
In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Yoshiro NaitoDepartment of Cardiovascular and Renal Medicine, School of Medicine, Hyogo Medical University, Nishinomiya, Japan. ynaito@hyo-med.ac.jp.
Hisashi SawadaSaha Cardiovascular Research Center, College of Medicine, University of Kentucky, Lexington, KY, USA.
Tetsuo HorimatsuDepartment of Cardiovascular and Renal Medicine, School of Medicine, Hyogo Medical University, Nishinomiya, Japan.
Masaki OhmurayaDepartment of Genetics, School of Medicine, Hyogo Medical University, Nishinomiya, Japan.
Masanori AsakuraDepartment of Cardiovascular and Renal Medicine, School of Medicine, Hyogo Medical University, Nishinomiya, Japan.
Masaharu IshiharaDepartment of Cardiovascular and Renal Medicine, School of Medicine, Hyogo Medical University, Nishinomiya, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transferrin receptor 1 (TfR1), a crucial cellular iron receptor, has a variety of biological functions. We have previously reported that TfR1 abundance increases in the aortic media of hypertensive rat models. However, its role in vascular diseases remains unknown. In the present study, we generated smooth muscle cell (SMC)-specific TfR1 deficient mice and examined the impact of its deletion in mouse models of hypertension induced by angiotensin II or deoxycorticosterone acetate/salt administration. SMC-specific TfR1 deletion attenuated medial thickening and elastin fragmentation in both mouse models of hypertension. These results indicate that TfR1 in SMCs exerts a role in vascular remodeling in hypertension.

Indexed as

HypertensionMuscle, Smooth, VascularMyocytes, Smooth MuscleReceptors, TransferrinVascular RemodelingAngiotensin IIAnimalsDesoxycorticosterone AcetateDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, KnockoutAngiotensin IIDesoxycorticosterone AcetateReceptors, TransferrinTfrc protein, mouseSmooth muscle cellTransferrin receptor 1Vascular remodeling

Identifiers

PMID40490490
PMCPMC12321566

What OpenQuestion holds

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Registered trials

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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.