Evidence map›Paper›PMID 36514868›Full record

ArticleAging cell2023

Dissecting the influence of cellular senescence on cell mechanics and extracellular matrix formation in vitro.

Erik Brauer, Tobias Lange, Daniela Keller, Sophie Görlitz, Simone Cho, Jacqueline Keye, Manfred Gossen, Ansgar Petersen, Uwe Kornak

Open access · goldFull text read
In one paragraph

Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 41 citations in OpenAlex.

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  8. Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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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 4 institutions in 1 country.

Erik BrauerJulius Wolff Institute, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.ORCID 0000-0002-5840-0520
Tobias LangeJulius Wolff Institute, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.
Daniela KellerInstitute for Medical Genetics and Human Genetics, Charité - Universtitätsmedizin Berlin, Berlin, Germany.
Sophie GörlitzJulius Wolff Institute, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.
Simone ChoJulius Wolff Institute, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.
Jacqueline KeyeFlow & Mass Cytometry Core Facility, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.
Manfred GossenBIH Center for Regenerative Therapies (BCRT), Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.
Ansgar PetersenJulius Wolff Institute, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany.
Uwe KornakInstitute for Medical Genetics and Human Genetics, Charité - Universtitätsmedizin Berlin, Berlin, Germany.
Berlin Institute of Health at Charité - Universitätsmedizin Berlin · DECharité - Universitätsmedizin Berlin · DEHelmholtz-Zentrum Hereon · DEUniversitätsmedizin Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue formation and healing both require cell proliferation and migration, but also extracellular matrix production and tensioning. In addition to restricting proliferation of damaged cells, increasing evidence suggests that cellular senescence also has distinct modulatory effects during wound healing and fibrosis. Yet, a direct role of senescent cells during tissue formation beyond paracrine signaling remains unknown. We here report how individual modules of the senescence program differentially influence cell mechanics and ECM expression with relevance for tissue formation. We compared DNA damage-mediated and DNA damage-independent senescence which was achieved through over-expression of either p16

Indexed as

Cellular SenescenceCyclin-Dependent Kinase Inhibitor p16Cell ProliferationCyclin-Dependent Kinase Inhibitor p21Extracellular MatrixHumansCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21cell forcecellular senescencecollagenextracellular matrixtissue regenerationwound contraction

Identifiers

PMID36514868
PMCPMC10014055
OpenAlexW4311357001

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read90
table measurements read15
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.