Evidence map›Paper›PMID 31098949›Full record

ArticleGeroScience2020

A pro longevity role for cellular senescence.

Amany Attaallah, Monia Lenzi, Silvia Marchionni, Giacomo Bincoletto, Veronica Cocchi, Eleonora Croco, Patrizia Hrelia, Silvana Hrelia, Christian Sell, Antonello Lorenzini

Open access · bronzeAbstract read
In one paragraph

Article in GeroScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  14. Review
  15. Article
  16. Bcl-xL as a Modulator of Senescence and Aging.International journal of molecular sciences · 2021
    Review
  17. Article
  18. Are We Ill Because We Age?Frontiers in physiology · 2019
    Review
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

10 authors at 3 institutions in 3 countries.

Amany AttaallahDepartment of Zoology, Faculty of Science, Damanhūr University, Damanhūr, 22511, Egypt.
Monia LenziDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Via San Donato 15, 40127, Bologna, Italy.
Silvia MarchionniDepartment of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna, Via Irnerio 48, 40126, Bologna, Italy.
Giacomo BincolettoDepartment of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna, Via Irnerio 48, 40126, Bologna, Italy.
Veronica CocchiDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Via San Donato 15, 40127, Bologna, Italy.
Eleonora CrocoDepartment of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna, Via Irnerio 48, 40126, Bologna, Italy.
Patrizia HreliaDepartment of Pharmacy and Biotechnology (FABIT), University of Bologna, Via San Donato 15, 40127, Bologna, Italy.
Silvana HreliaDepartment for Life Quality Studies, University of Bologna, C.so d'Augusto, 237, 47921, Rimini, Italy.
Christian SellDepartment of Pathology & Laboratory Medicine, Drexel University College of Medicine, 245 N. 15th Street, Philadelphia, PA, 19102, USA.
Antonello LorenziniDepartment of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna, Via Irnerio 48, 40126, Bologna, Italy. antonello.lorenzini@unibo.it.ORCID 0000-0001-9615-9697
University of Bologna · ITDrexel University · USDamanhour University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is a fundamental process that may play positive or detrimental roles for the organism. It is involved in tissue development and in tumor prevention although during aging is becoming a detrimental process contributing to the decline of tissue functions. In previous investigations, we have uncovered a better capacity to detect DNA damage in cells from long-lived mammals. Here, we report that cultured cells derived from long-lived species have a higher propensity to undergo senescence when challenged with DNA damage than cells derived from short-lived species. Using a panel of cells derived from six mammals, which range in lifespan from 3-4 years up to 120 years, we examined cell cycle response, induction of apoptosis and of cellular senescence. All species exhibited a cell cycle arrest while induction of apoptosis was variable. However, a significant positive correlation was found between the relative percent of cells, within a population which entered senescence following damage, and the lifespan of the species. We suggest that cellular senescence may have a positive role during development allowing it to contribute to the evolution of longevity.

Indexed as

Cellular SenescenceLongevityAgingAnimalsbeta-GalactosidaseDNA Damagebeta-GalactosidaseApoptosisBody massCellular senescenceLongevitySA β-gal

Identifiers

PMID31098949
PMCPMC7286999
OpenAlexW2946804491

What OpenQuestion holds

Textmetadata
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.