Evidence map›Paper›PMID 41227316›Full record

ArticleCells2025

Caspase-6 Is a Non-Apoptotic Effector of Shear-Induced Morphological Adaptation in Pulmonary Artery Endothelial Cells In Vitro.

Corey Wittig, Emir Bora Akmeriç, Laura Michalick, Jakob M König, Wolfgang M Kuebler, Holger Gerhardt, Robert Szulcek

Abstract read
In one paragraph

Article in Cells, 2025. 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

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

7 authors.

Corey WittigLaboratory of In Vitro Modeling Systems of Pulmonary and Thrombotic Diseases, Institute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.ORCID 0000-0003-4296-9293
Emir Bora AkmeriçCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universitätsmedizin Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.ORCID 0000-0003-4463-8017
Laura MichalickInstitute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universitätsmedizin Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.ORCID 0000-0002-3959-5828
Jakob M KönigLaboratory of In Vitro Modeling Systems of Pulmonary and Thrombotic Diseases, Institute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.
Wolfgang M KueblerInstitute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universitätsmedizin Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.ORCID 0000-0003-4100-2961
Holger GerhardtCharité-Universitätsmedizin Berlin, Corporate Member of Freie Universitätsmedizin Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.ORCID 0000-0002-3030-0384
Robert SzulcekLaboratory of In Vitro Modeling Systems of Pulmonary and Thrombotic Diseases, Institute of Physiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, 10117 Berlin, Germany.ORCID 0000-0003-0450-7338

Funding

Deutsche Forschungsgemeinschaft SFB 1470, project ID 437531118, sub-project A04; operational grants KU1218/12-1, KU1218/14-1Fondation Leducq 17 CVD 03German Centre for Cardiovascular Research 81Z0100214Open Access Publication Fund of Charité - Universitätsmedizin Berlin and the German Research Foundation (DFG) na
6 · The paper itself

Abstract

Caspases are known for their roles in cell death and inflammation. However, emerging evidence suggests they also mediate non-lethal processes, governed by a finely tuned balance of localization, activity, kinetics, and substrate availability. Given that many caspase substrates are implicated in mechanoadaptive processes, we investigated if caspases contribute to morphological adaptation of human pulmonary artery endothelial cells to fluid shear stress and other morphology-altering stimuli in vitro. Using selective inhibitors, we screened all major caspases for a role in endothelial cell adaptation to unidirectional laminar shear stress (15 dyn/cm

Indexed as

Adaptation, PhysiologicalCaspase 6Endothelial CellsPulmonary ArteryStress, MechanicalApoptosisHumansCaspase 6caspase-6caspasesendothelial cellsfluid flowmechanoadaptationmechanotransductionmorphological adaptationshear stressvascular biology

Identifiers

PMID41227316
PMCPMC12609614

What OpenQuestion holds

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LicenceCC BY
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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.