Evidence map›Paper›PMID 33809739›Full record

ArticleCells2021

Piezo1 Channels Contribute to the Regulation of Human Atrial Fibroblast Mechanical Properties and Matrix Stiffness Sensing.

Ramona Emig, Wiebke Knodt, Mario J Krussig, Callum M Zgierski-Johnston, Oliver Gorka, Olaf Groß, Peter Kohl, Ursula Ravens, Rémi Peyronnet

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
7.6field-weighted citation impact, top 2% of its field
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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

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  20. CaBiomedicines · 2025
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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

9 authors at 1 institution in 1 country.

Ramona EmigInstitute for Experimental Cardiovascular Medicine, University Heart Center Freiburg Bad Krozingen, and Faculty of Medicine, University of Freiburg, 79110 Freiburg, Germany.
Wiebke KnodtInstitute for Experimental Cardiovascular Medicine, University Heart Center Freiburg Bad Krozingen, and Faculty of Medicine, University of Freiburg, 79110 Freiburg, Germany.
Mario J KrussigInstitute for Experimental Cardiovascular Medicine, University Heart Center Freiburg Bad Krozingen, and Faculty of Medicine, University of Freiburg, 79110 Freiburg, Germany.
Callum M Zgierski-JohnstonInstitute for Experimental Cardiovascular Medicine, University Heart Center Freiburg Bad Krozingen, and Faculty of Medicine, University of Freiburg, 79110 Freiburg, Germany.ORCID 0000-0002-6773-9884
Oliver GorkaInstitute of Neuropathology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0000-0002-8245-3008
Olaf GroßInstitute of Neuropathology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0000-0001-8660-3619
Peter KohlInstitute for Experimental Cardiovascular Medicine, University Heart Center Freiburg Bad Krozingen, and Faculty of Medicine, University of Freiburg, 79110 Freiburg, Germany.
Ursula RavensInstitute for Experimental Cardiovascular Medicine, University Heart Center Freiburg Bad Krozingen, and Faculty of Medicine, University of Freiburg, 79110 Freiburg, Germany.
Rémi PeyronnetInstitute for Experimental Cardiovascular Medicine, University Heart Center Freiburg Bad Krozingen, and Faculty of Medicine, University of Freiburg, 79110 Freiburg, Germany.ORCID 0000-0002-5708-6410
University of Freiburg · DE

Funding

Deutsche Forschungsgemeinschaft 390939984Deutsche Forschungsgemeinschaft 422681845European Research Council 337689
6 · The paper itself

Abstract

The mechanical environment of cardiac cells changes continuously and undergoes major alterations during diseases. Most cardiac diseases, including atrial fibrillation, are accompanied by fibrosis which can impair both electrical and mechanical function of the heart. A key characteristic of fibrotic tissue is excessive accumulation of extracellular matrix, leading to increased tissue stiffness. Cells are known to respond to changes in their mechanical environment, but the molecular mechanisms underlying this ability are incompletely understood. We used cell culture systems and hydrogels with tunable stiffness, combined with advanced biophysical and imaging techniques, to elucidate the roles of the stretch-activated channel Piezo1 in human atrial fibroblast mechano-sensing. Changing the expression level of Piezo1 revealed that this mechano-sensor contributes to the organization of the cytoskeleton, affecting mechanical properties of human embryonic kidney cells and human atrial fibroblasts. Our results suggest that this response is independent of Piezo1-mediated ion conduction at the plasma membrane, and mediated in part by components of the integrin pathway. Further, we show that Piezo1 is instrumental for fibroblast adaptation to changes in matrix stiffness, and that Piezo1-induced cell stiffening is transmitted in a paracrine manner to other cells by a signaling mechanism requiring interleukin-6. Piezo1 may be a new candidate for targeted interference with cardiac fibroblast function.

Indexed as

Mechanotransduction, CellularCytoskeletonElastic ModulusExtracellular MatrixFibroblastsFibrosisHeart AtriaHEK293 CellsHumansIntegrin beta1Interleukin-6Ion ChannelsParacrine CommunicationIL6 protein, humanIntegrin beta1Interleukin-6Ion ChannelsItgb1 protein, humanPIEZO1 protein, humanactinadhesioncalpaincardiac fibrosiscytoskeletonFAKheartintegrinROCKYoung’s modulus

Identifiers

PMID33809739
PMCPMC8002259
OpenAlexW3137728895

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.