In one paragraphArticle in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
5 · Who and what moneyAuthors and funding
7 authors.
Alexandra N RindoneTranslational Tissue Engineering Center, Wilmer Eye Institute and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0003-2291-5933 Ya GuanDepartment of Biomedical Engineering, Duke University, Durham, North Carolina, USA.
Connor D AmelungDepartment of Biomedical Engineering, Duke University, Durham, North Carolina, USA.
Prarthana Sanjay DaswaniTranslational Tissue Engineering Center, Wilmer Eye Institute and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, USA.
Jennifer H ElisseeffTranslational Tissue Engineering Center, Wilmer Eye Institute and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, USA.ORCID https://orcid.org/0000-0002-5066-1996 Funding
Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI ALAN KEITH MEEKER · 1985 to 2026
$208.6MWomen's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI Laura Fish · 1985 to 2026
$174.8MRegional Biocontainment Laboratory (RBL)UC6AI058607 · NIAID · DUKE UNIVERSITY · PI WILLIAMS, R SANDERS · 2003 to 2005
$16.3MResources and Workforce Development for the Regional Biocontainment LaboratoriesUC7AI180254 · NIAID · DUKE UNIVERSITY · PI Herman F Staats · 2023 to 2026
$14.0MRegional Biocontainment Laboratories Facility and Building System Upgrades SupportG20AI167200 · NIAID · DUKE UNIVERSITY · PI STAATS, HERMAN F · 2021 to 2022
$6.6MJHU-Mayo-NIA Murine Senescence Mapping Program (JMN-MSMP)U54AG079779 · NIA · JOHNS HOPKINS UNIVERSITY · PI Darren Baker, JENNIFER H ELISSEEFF · 2022 to 2026
$6.4MSenescence in the Foreign Body Response Across LifespanR01AG082965 · NIA · JOHNS HOPKINS UNIVERSITY · PI JENNIFER H ELISSEEFF · 2024 to 2026
$2.0MEngineering three-dimensional perfusable microphysiological models of the human inner blood-retina barrierR01EY035853 · NEI · DUKE UNIVERSITY · PI Sharon Gerecht · 2024 to 2026
$1.9MAmerican Heart AssociationBloomberg ∼ Kimmel InstituteDuke Science and Technology National Institute of Health NIH U54AG079779Duke Science and Technology National Institute of Health R01AG082965Duke Science and Technology National Institute of Health R01EY035853Mandel Foundation, Duke Regeneration Center (DRC)National Science Foundation Graduate Research Fellowship Program NSF GRFPNCI NIH HHS P30 CA006973NCI NIH HHS P30 CA014236NEI NIH HHS R01 EY035853NIAID NIH HHS G20 AI167200NIAID NIH HHS UC6 AI058607NIAID NIH HHS UC7 AI180254NIA NIH HHS R01 AG082965NIA NIH HHS U54 AG079779
6 · The paper itselfAbstract
Identifying the drivers of cellular senescence that contribute to the decline in vascular function with age and disease is critical for developing restorative interventions. Here, we investigated how increased mechanical stress from extracellular matrix (ECM) stiffening shapes endothelial cell (EC) senescence. We developed a 3D human in vitro model that decouples mechanical stress from inflammatory or biochemical signals, enabling the study of senescence responses to tissue stiffening alone. We found that matrix stiffening induces an EC senescence phenotype with elevated p16/p21 and an immunomodulatory senescence-associated secretory phenotype (SASP), in the absence of inflammatory signals. This mechano-induced senescence activates Notch signaling, and treatment with an FDA-approved γ-secretase inhibitor attenuates stiffness-induced senescence. Analysis of fibrotic capsule tissue from patients with synthetic breast implants, a model of localized, mechanically driven fibrosis, validated an increase in p16
Indexed as
Cellular SenescenceEndothelial CellsExtracellular MatrixCells, CulturedHumansSenescence-Associated Secretory PhenotypeSignal TransductionStress, Mechanicalbiomaterialcell biologyendothelial stem cellengineered tissueextracellular matrixfibrosishydrogel scaffoldnotch signaling pathwayphenotypesenescence
Identifiers
PMID42389866
PMCPMC13337105
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