Evidence map›Paper›PMID 34344977›Full record

ArticleScientific reports2021

Acute ischemic stroke triggers a cellular senescence-associated secretory phenotype.

Coral Torres-Querol, Pascual Torres, Noemí Vidal, Manel Portero-Otín, Gloria Arque, Francisco Purroy

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  18. Therapeutic targeting of senescent cells in the CNS.Nature reviews. Drug discovery · 2024
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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

6 authors at 3 institutions in 1 country.

Coral Torres-Querol *Clinical Neurosciences Group, Institut de Recerca Biomèdica de Lleida (IRBLleida), Lleida, Spain.
Pascual Torres *Experimental Medicine Department, Universitat de Lleida, Institut de Recerca Biomèdica de Lleida (IRBLleida), Lleida, Spain.
Noemí VidalDepartment of Pathology, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Barcelona, Spain.
Manel Portero-OtínExperimental Medicine Department, Universitat de Lleida, Institut de Recerca Biomèdica de Lleida (IRBLleida), Lleida, Spain.
Gloria ArqueClinical Neurosciences Group, Institut de Recerca Biomèdica de Lleida (IRBLleida), Lleida, Spain.
Francisco PurroyClinical Neurosciences Group, Institut de Recerca Biomèdica de Lleida (IRBLleida), Lleida, Spain. fpurroygarcia@gmail.com.
Biomedical Research Institute of Lleida · ESUniversitat de Lleida · ESBellvitge University Hospital · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senescent cells are capable of expressing a myriad of inflammatory cytokines and this pro-inflammatory phenomenon is known as senescence-associated secretory phenotype (SASP). The contribution of this phenomenon in brain ischemia was scarce. A mouse model of transient focal cerebral ischemia by compressing the distal middle cerebral artery (tMCAo) for 60 min was used. SASP, pro-inflammatory cytokines and cell cycle mRNAs levels were quantified at 30-min and 72 h post-surgery. Immunohistochemistry in paraffin embedded human brain slides and mouse brain tissue was performed. Our results showed an increase of both p16 and p21 mRNA restricted to the infarct area in the tMCAo brain. Moreover, there was an induction of Il6, Tnfa, Cxc11, and its receptor Cxcr2 mRNA pro-inflammatory cytokines with a high positive correlation with p16/p21 mRNA levels. The p16 was mainly shown in cytoplasm of neurons and cytoplasm/membrane of microglial cells. The p21 was observed in membrane of neurons and also it showed a mixed cytoplasmic and membranous pattern in the microglial cells. In a human stroke patient, an increase of P16 in the perimeter of the MCA infarct area was observed. These suggest a role of SASP in tMCAo mouse model and in human brain tissue. SASP potentially has a physiological role in acute ischemic stroke and neurological function loss.

Indexed as

Cellular SenescenceDisease Models, AnimalPhenotypeAgedAnimalsBiomarkersBrain IschemiaCell CycleGene Expression RegulationHumansInfarction, Middle Cerebral ArteryIschemic StrokeMaleMiceMiddle AgedBiomarkers

Identifiers

PMID34344977
PMCPMC8333348
OpenAlexW3190156496

What OpenQuestion holds

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LicenceCC BY
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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.