ArticleAging2014
Gerosuppression in confluent cells.
Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- A Signature of Senescence Based on An Analysis of Selected Markers in Primary Vascular Smooth Muscle Cells Cultured In Vitro and Derived from Atherosclerotic Plaque.Aging and disease · 2025Article
- NIH SenNet Consortium to map senescent cells throughout the human lifespan to understand physiological health.Nature aging · 2022Article
- S6 kinase 1 at the central node of cell size and ageing.Frontiers in cell and developmental biology · 2022Review
- Cellular aging beyond cellular senescence: Markers of senescence prior to cell cycle arrest in vitro and in vivo.Aging cell · 2021Review
- Review
- Article
- Autophagic processes increase during senescence in cultured sheep neurons and astrocytes.European journal of histochemistry : EJH · 2018Article
- Rapamycin, proliferation and geroconversion to senescence.Cell cycle (Georgetown, Tex.) · 2018Article
- A small molecule inhibitor of PAI-1 protects against doxorubicin-induced cellular senescence.Oncotarget · 2016Article
- Article
- Inhibitors of mTOR in aging and cancer.Oncotarget · 2015Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The most physiological type of cell cycle arrest - namely, contact inhibition in dense culture - is the least densely studied. Despite cell cycle arrest, confluent cells do not become senescent. We recently described that mTOR (target of rapamycin) is inactive in contact-inhibited cells. Therefore, conversion from reversible arrest to senescence (geroconversion) is suppressed. I this Perspective, we further extended the gerosuppression model. While causing senescence in regular cell density, etoposide failed to cause senescence in contact-inhibited cells. A transient reactivation of mTOR favored geroconversion in etoposide-treated confluent cells. Like p21, p16 did not cause senescence in high cell density. We discuss that suppression of geroconversion in confluent and contact-inhibited cultures mimics gerosuppression in the organism. We confirmed that levels of p-S6 were low in murine tissues in the organism compared with mouse embryonic fibroblasts in cell culture, whereas p-Akt was reciprocally high in the organism.
Indexed as
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What OpenQuestion holds
Registered trials
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.