Evidence map›Paper›PMID 33546395›Full record

ReviewInternational journal of molecular sciences2021

Bcl-xL as a Modulator of Senescence and Aging.

Cristina Mas-Bargues, Consuelo Borrás, Jose Viña

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Infection and immunity · 2026
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  20. The emerging roles of NFrontiers in molecular neuroscience · 2022
    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 1 country.

Cristina Mas-BarguesFreshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia, Centro de Investigación Biomédica en Red Fragilidad y Envejecimiento Saludable-Instituto de Salud Carlos III (CIBERFES-ISCIII), Instituto Sanitario de Investigación INCLIVA, 46010 Valencia, Spain.ORCID 0000-0003-1131-1894
Consuelo BorrásFreshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia, Centro de Investigación Biomédica en Red Fragilidad y Envejecimiento Saludable-Instituto de Salud Carlos III (CIBERFES-ISCIII), Instituto Sanitario de Investigación INCLIVA, 46010 Valencia, Spain.ORCID 0000-0003-4606-1792
Jose ViñaFreshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia, Centro de Investigación Biomédica en Red Fragilidad y Envejecimiento Saludable-Instituto de Salud Carlos III (CIBERFES-ISCIII), Instituto Sanitario de Investigación INCLIVA, 46010 Valencia, Spain.ORCID 0000-0001-9709-0089
Universitat de València · ES

Funding

Conselleria d'Educació, Investigació, Cultura i Esport APOSTD/2018/230Conselleria d'Educació, Investigació, Cultura i Esport PROMETEO/2019/097European Commission JPI HDHL INTIMIC-085H2020 European Research Council ERA-HDHL GA N° 696295H2020 European Research Council H2020- DIABFRAIL-LATAM (Ref: 825546)Instituto de Salud Carlos III CB16/10/00435Ministerio de Ciencia e Innovación PCIN-2017-117Ministerio de Ciencia e Innovación PID2019-110906RB-I00/AEI/10.13039/501100011033
6 · The paper itself

Abstract

Many features of aging result from the incapacity of cells to adapt to stress conditions. When cells are overwhelmed by stress, they can undergo senescence to avoid unrestricted growth of damaged cells. Recent findings have proven that cellular senescence is more than that. A specific grade of senescence promotes embryo development, tissue remodeling and wound healing. However, constant stresses and a weakening immune system can lead to senescence chronicity with aging. The accumulation of senescent cells is directly related to tissue dysfunction and age-related pathologies. Centenarians, the most aged individuals, should accumulate senescent cells and suffer from their deleterious effects, however, they enjoy a compression of morbidity. We have shown that they overexpress B-cell lymphoma-extra large (Bcl-xL). Bcl-xL could avoid an excessive burden of senescent cells through the regulation of intrinsic apoptosis, mitochondrial bioenergetics and oxidative stress. On the other hand, Bcl-xL maintains a fully functional immune system that ensures an efficient clearance of senescent cells. Moreover, there is a paradox, as inhibitors of Bcl-xL have been employed as senolytic agents, which have been shown to protect from aging in animal models. In this review, we aim to discuss how Bcl-xL could modulate senescence-associated harmful effects in centenarians, protecting them from the burden of accumulation of senescent cells.

Indexed as

Cellular SenescenceAgingAnimalsApoptosisbcl-X ProteinBiomarkersDisease SusceptibilityDNA DamageGene Expression RegulationHumansImmunologic SurveillanceOrgan SpecificityProtein BindingSignal TransductionStress, Physiologicalbcl-X ProteinBiomarkersagingapoptosisBcl-xLcentenariansimmunosenescencesenescencesenolytics

Identifiers

PMID33546395
PMCPMC7913597
OpenAlexW3128379228

What Socratic 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 Socratic graph.