Evidence map›Paper›PMID 39494438›Full record

ArticleFujita medical journal2024

Phosphate overload via the type III Na-dependent Pi transporter represses aortic wall elastic fiber formation.

Yasumasa Yoshino, Tomoka Hasegawa, Shukei Sugita, Eisuke Tomatsu, Naoya Murao, Izumi Hiratsuka, Sahoko Sekiguchi-Ueda, Megumi Shibata, Takeo Matsumoto, Norio Amizuka and 4 more

Abstract read
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In one paragraph

Article in Fujita medical journal, 2024. 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

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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

14 authors.

Yasumasa YoshinoDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Tomoka HasegawaDepartment of Developmental Biology of Hard Tissue, Division of Oral Health Science, Graduate School of Dental Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
Shukei SugitaBiomechanics Laboratory, Nagoya Institute of Technology, Nagoya, Aichi, Japan.
Eisuke TomatsuDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Naoya MuraoDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Izumi HiratsukaDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Sahoko Sekiguchi-UedaDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Megumi ShibataDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Takeo MatsumotoDepartment of Mechanical Systems and Engineering, Graduate School of Engineering, Nagoya University, Nagoya, Aichi, Japan.
Norio AmizukaDepartment of Developmental Biology of Hard Tissue, Division of Oral Health Science, Graduate School of Dental Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
Yusuke SeinoDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Takeshi TakayanagiDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Yoshihisa SugimuraDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.
Atsushi SuzukiDepartment of Endocrinology, Diabetes and Metabolism, Fujita Health University, School of Medicine, Toyoake, Aichi, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: Phosphate (Pi) induces differentiation of arterial smooth muscle cells to the osteoblastic phenotype by inducing the type III Na-dependent Pi transporter Pit-1/solute carrier family member 1. This induction can contribute to arterial calcification, but precisely how Pi stress acts on the vascular wall remains unclear. We investigated the role of extracellular Pi in inducing microstructural changes in the arterial wall. Methods: Aortae of Pit-1-overexpressing transgenic (TG) rats and their wild-type (WT) littermates were obtained at 8 weeks after birth. The thoracic descending aorta from WT and TG rats was used for the measurement of wall thickness and uniaxial tensile testing. Structural and ultrastructural analyses were performed using light microscopy and transmission electron microscopy. Gene expression of connective tissue components in the aorta was quantified by quantitative real-time polymerase chain reaction. Results: Aortic wall thickness in TG rats was the same as that in WT rats. Uniaxial tensile testing showed that the circumferential breaking stress in TG rats was significantly lower than that in WT rats ( Conclusions: Pi overload acting via the arterial wall Pit-1 transporter weakens circumferential strength by causing elastic fiber malformation, probably via decreased fibrillin-1 expression.

Indexed as

AortaAtherosclerosisElastinFibrillinPhosphate

Identifiers

PMID39494438
PMCPMC11528329

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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.