Evidence map›Paper›PMID 32182711›Full record

ReviewBiomolecules2020

Role of p53 in the Regulation of Cellular Senescence.

Mahmut Mijit, Valentina Caracciolo, Antonio Melillo, Fernanda Amicarelli, Antonio Giordano

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 373 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
373citing papers in PubMed, 2 pooled it
33.2field-weighted citation impact, top 1% 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

373 citing papers in PubMed, 2 syntheses or guidelines pooled it, 581 citations in OpenAlex.

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313 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

Mahmut MijitSbarro Institute for Cancer Research and Molecular Medicine, Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA.
Valentina CaraccioloSbarro Institute for Cancer Research and Molecular Medicine, Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA.
Antonio MelilloSbarro Institute for Cancer Research and Molecular Medicine, Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA.
Fernanda AmicarelliDepartment of Medical Biotechnologies, University of Siena, 67100 Siena, Italy.
Antonio GiordanoSbarro Institute for Cancer Research and Molecular Medicine, Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA.ORCID 0000-0002-5959-016X
Temple University · USUniversity of Siena · ITUniversity of L'Aquila · IT

Funding

Commonwealth of Pennsylvania, Department of Health 290228/13650H2020 Marie Skłodowska-Curie Actions 713714
6 · The paper itself

Abstract

The p53 transcription factor plays a critical role in cellular responses to stress. Its activation in response to DNA damage leads to cell growth arrest, allowing for DNA repair, or directs cellular senescence or apoptosis, thereby maintaining genome integrity. Senescence is a permanent cell-cycle arrest that has a crucial role in aging, and it also represents a robust physiological antitumor response, which counteracts oncogenic insults. In addition, senescent cells can also negatively impact the surrounding tissue microenvironment and the neighboring cells by secreting pro-inflammatory cytokines, ultimately triggering tissue dysfunction and/or unfavorable outcomes. This review focuses on the characteristics of senescence and on the recent advances in the contribution of p53 to cellular senescence. Moreover, we also discuss the p53-mediated regulation of several pathophysiological microenvironments that could be associated with senescence and its development.

Indexed as

Cell Cycle CheckpointsCellular MicroenvironmentCellular SenescenceDNA DamageDNA RepairAnimalsHumansTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53cell cycle arrestDNA damagemicroenvironmentp53senescence

Identifiers

PMID32182711
PMCPMC7175209
OpenAlexW3010215457

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.