Evidence map›Paper›PMID 42713657›Full record

ArticleCirculation research2026

Mechanosensitive Stanniocalcin-1 Suppresses Smooth Muscle Cell Proliferation and Attenuates Experimental Pulmonary Hypertension.

Mariko Kogami, Yuko Kato, Satoko Ito, Keiko Uchida, Hana Inoue, Yuko Hidaka, Shota Tanifuji, Mayumi Yokotsuka, Yoshinari Yamamoto, Toshitaka Nagao and 4 more

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Article in Circulation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

14 authors.

Mariko KogamiDepartment of Physiology (M.K., Y.K., S.I., K.U., H.I., Y.H., U.Y.), Tokyo Medical University, Japan.ORCID 0000-0002-2637-7872
Yuko KatoDepartment of Physiology (M.K., Y.K., S.I., K.U., H.I., Y.H., U.Y.), Tokyo Medical University, Japan.ORCID 0000-0002-1535-1925
Satoko ItoDepartment of Physiology (M.K., Y.K., S.I., K.U., H.I., Y.H., U.Y.), Tokyo Medical University, Japan.
Keiko UchidaDepartment of Physiology (M.K., Y.K., S.I., K.U., H.I., Y.H., U.Y.), Tokyo Medical University, Japan.ORCID 0009-0004-9249-6345
Hana InoueDepartment of Physiology (M.K., Y.K., S.I., K.U., H.I., Y.H., U.Y.), Tokyo Medical University, Japan.ORCID 0000-0002-2278-5617
Yuko HidakaDepartment of Physiology (M.K., Y.K., S.I., K.U., H.I., Y.H., U.Y.), Tokyo Medical University, Japan.ORCID 0009-0000-3383-1589
Shota TanifujiDepartment of Anatomy (S.T.), Tokyo Medical University, Japan.ORCID 0009-0003-5145-1768
Mayumi YokotsukaDepartment of Anatomic Pathology (M.Y., Y.Y., T.N.), Tokyo Medical University, Japan.
Yoshinari YamamotoDepartment of Anatomic Pathology (M.Y., Y.Y., T.N.), Tokyo Medical University, Japan.
Toshitaka NagaoDepartment of Anatomic Pathology (M.Y., Y.Y., T.N.), Tokyo Medical University, Japan.ORCID 0000-0003-2075-9738
Shinji AbeDepartment of Respiratory Medicine (M.K., S.A.), Tokyo Medical University, Japan.
Roger R ReddelCancer Research Unit, Children's Medical Research Institute, Faculty of Medicine and Health, University of Sydney, Australia (R.R.R.).ORCID 0000-0002-6302-6107
Kazufumi NakamuraCenter for Advanced Heart Failure, Okayama University Hospital, Japan (K.N.).ORCID 0000-0001-8845-3626
Utako YokoyamaDepartment of Physiology (M.K., Y.K., S.I., K.U., H.I., Y.H., U.Y.), Tokyo Medical University, Japan.ORCID 0000-0003-1803-0155

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIdiopathic pulmonary arterial hypertension (IPAH) is driven by progressive vascular remodeling, particularly smooth muscle cell (SMC) proliferation. Current combination vasodilator therapies have markedly improved outcomes; however, prognosis remains poor in subgroups such as patients with respiratory comorbidities. Elevation of intravascular hydrostatic pressure is a hallmark of IPAH, yet its direct role in pulmonary artery SMCs remains unclear. We aimed to identify pressure-responsive mediators using a newly developed hydrostatic pressurization system to model hypertensive hemodynamics.

methodsPulmonary artery SMCs from 4 patients with IPAH were exposed to high hydrostatic pressure (70/40 mm Hg, 60 bpm). Transcriptomic profiling identified differentially expressed genes, which were validated by quantitative polymerase chain reaction. Functional studies included PIEZO1 (piezo type mechanosensitive ion channel component 1) modulation, rhSTC1 (recombinant human stanniocalcin-1) treatment, bromodeoxyuridine incorporation, and Western blotting for cell-cycle regulators. Chronic hypoxia-induced pulmonary hypertension was assessed in wild-type and

resultsRNA sequencing revealed

conclusionsElevated hydrostatic pressure drives

Indexed as

Cell ProliferationFamilial Primary Pulmonary HypertensionGlycoproteinsMechanotransduction, CellularMuscle, Smooth, VascularMyocytes, Smooth MuscleAnimalsCells, CulturedDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutPulmonary ArteryGlycoproteinsteleocalcincell proliferationmechanotransduction, cellularpulmonary arterial hypertensionstanniocalcin-1

Identifiers

PMID42713657
PMCPMC13649279

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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.