Evidence map›Paper›PMID 39745817›Full record

ArticleThe Journal of clinical endocrinology and metabolism2025

Stimulation of Piezo1 Mechanosensitive Channels Inhibits Adipogenesis in Thyroid Eye Disease.

Erika Galgoczi, Istvan Orsos, Zsanett Molnar, Bernadett Ujhelyi, Zita Steiber, Laszlo Szabo, Beatrix Dienes, Laszlo Csernoch, Endre V Nagy, Monika Katko

Abstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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

10 authors.

Erika GalgocziDivision of Endocrinology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.ORCID 0000-0002-1701-4623
Istvan OrsosDivision of Endocrinology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Zsanett MolnarDivision of Endocrinology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Bernadett UjhelyiDepartment of Ophthalmology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Zita SteiberDepartment of Ophthalmology, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Laszlo SzaboHUN-REN DE Cell Physiology Research Group, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Beatrix DienesHUN-REN DE Cell Physiology Research Group, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Laszlo CsernochHUN-REN DE Cell Physiology Research Group, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Endre V NagyDivision of Endocrinology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.ORCID 0000-0002-9286-6471
Monika KatkoDivision of Endocrinology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.

Funding

Hungarian National Research, Development and Innovation Office K143464Ministry of Innovation and Technology of HungaryNational Research, Development and Innovation Fund K_22
6 · The paper itself

Abstract

contextIncreased orbital tissue volume due to matrix expansion, orbital fibroblast (OF) proliferation, and adipocyte differentiation are the hallmarks of thyroid eye disease (TED). Their combination with the presence of hyaluronan-bound excess water in the constrains of the bony orbit results in increased intraorbital pressure. High intraorbital pressure, along with changes in the mechanical properties of orbital tissues, may lead to the activation of mechanosensitive receptors. The expression and role of the Piezo1 mechanoreceptor has not been investigated in TED.

objectiveWe aimed to verify the expression of Piezo1 in OFs, and to study the effect of in vitro Piezo1 activation by its synthetic agonist Yoda1 on adipocyte differentiation.

methodsOF cultures established using orbital connective tissues from patients with TED and controls were studied in the presence or absence of adipogenic stimuli. Piezo1 expression was confirmed by Western Blot and immunofluorescent imaging, and its function was verified by intracellular Ca2+ measurement. Adipogenic differentiation was characterized using Oil Red O staining for lipid accumulation, real-time polymerase chain reaction for gene and Western blot for protein expressions indicative in adipogenesis.

resultsOFs express functional Piezo1 channels. Differentiation into adipocytes is inherent to TED OFs. Piezo1 activation by Yoda1 inhibits the expressions of early (CEBPβ, CEBPδ) and main (PPARγ, CEBPα) transcription factors, and the terminal marker FABP4 during adipogenesis, resulting in markedly lower intracytoplasmic lipid accumulation.

conclusionPiezo1 channels are expressed and functional in OFs. Modeling orbital pressure by in vitro Piezo1 activation reduces de novo adipogenesis of OFs derived from TED orbits.

Indexed as

AdipogenesisGraves OphthalmopathyIon ChannelsAdipocytesAdultCell DifferentiationCells, CulturedFemaleFibroblastsHumansMaleMechanotransduction, CellularMiddle AgedOrbitPyrazinesThiadiazolesIon ChannelsPIEZO1 protein, humanPyrazinesThiadiazolesyoda-1adipogenesisGraves orbitopathyorbital fibroblastsPiezo1PPARγYoda1

Identifiers

PMID39745817
PMCPMC12342356

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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.