Evidence map›Paper›PMID 33378554›Full record

ReviewNeuropathology and applied neurobiology2021

Cell senescence in neuropathology: A focus on neurodegeneration and tumours.

Gabriela Carreno, Romain Guiho, Juan Pedro Martinez-Barbera

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuropathology and applied neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 76 citations in OpenAlex.

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  20. MOST wanted: navigating the MAPK-OIS-SASP-tumor microenvironment axis in primary pediatric low-grade glioma and preclinical models.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2024
    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

3 authors at 1 institution in 2 countries.

Gabriela CarrenoDevelopmental Biology and Cancer Programme, Birth Defects Research Centre, Institute of Child Health Great Ormond Street Hospital, University College London, 30 Guilford Street, London, WC1N 1EH, UK.ORCID 0000-0003-4725-6225
Romain GuihoDevelopmental Biology and Cancer Programme, Birth Defects Research Centre, Institute of Child Health Great Ormond Street Hospital, University College London, 30 Guilford Street, London, WC1N 1EH, UK.ORCID 0000-0002-9231-6445
Juan Pedro Martinez-BarberaDevelopmental Biology and Cancer Programme, Birth Defects Research Centre, Institute of Child Health Great Ormond Street Hospital, University College London, 30 Guilford Street, London, WC1N 1EH, UK.ORCID 0000-0002-5292-7276
Great Ormond Street Hospital · GB

Funding

Cancer Research UK 27727Department of HealthMedical Research Council MR/M000125/1
6 · The paper itself

Abstract

The study of cell senescence is a burgeoning field. Senescent cells can modify the cellular microenvironment through the secretion of a plethora of biologically active products referred to as the senescence-associated secretory phenotype (SASP). The consequences of these paracrine signals can be either beneficial for tissue homeostasis, if senescent cells are properly cleared and SASP activation is transient, or result in organ dysfunction, when senescent cells accumulate within the tissues and SASP activation is persistent. Several studies have provided evidence for the role of senescence and SASP in promoting age-related diseases or driving organismal ageing. The hype about senescence has been further amplified by the fact that a group of drugs, named senolytics, have been used to successfully ameliorate the burden of age-related diseases and increase health and life span in mice. Ablation of senescent cells in the brain prevents disease progression and improves cognition in murine models of neurodegenerative conditions. The role of senescence in cancer has been more thoroughly investigated, and it is now accepted that senescence is a double-edged sword that can paradoxically prevent or promote tumourigenesis in a context-dependent manner. In addition, senescence induction followed by senolytic treatment is starting to emerge as a novel therapeutic avenue that could improve current anti-cancer therapies and reduce tumour recurrence. In this review, we discuss recent findings supporting the role of cell senescence in the pathogenesis of neurodegenerative diseases and in brain tumours. A better understanding of senescence is likely to result in the development of novel and efficacious anti-senescence therapies against these brain pathologies.

Indexed as

AnimalsBrain NeoplasmsCarcinogenesisCellular SenescenceHumansNerve DegenerationAlzheimer's diseasecell senescencecraniopharyngiomadiffuse midline gliomaglioblastoma multiformelow-grade gliomamedulloblastomamultiple sclerosisParkinson's diseaseSASPsenolytic

Identifiers

PMID33378554
PMCPMC8603933
OpenAlexW3116069652

What OpenQuestion holds

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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.