Evidence map›Paper›PMID 37466640›Full record

ArticleAge and ageing2023

New Horizons in cellular senescence for clinicians.

Miles D Witham, Antoneta Granic, Satomi Miwa, Joao F Passos, Gavin D Richardson, Avan A Sayer

Open access · hybridAbstract read
In one paragraph

Article in Age and ageing, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Malnutrition in Obesity: When BMI-Based Screening Masks Clinical Risk.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Sarcopenia.Nature reviews. Disease primers · 2024
    Review
  9. Review
  10. Article
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 4 institutions in 2 countries.

Miles D WithamAGE Research Group, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, UK.
Antoneta GranicAGE Research Group, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, UK.
Satomi MiwaBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, UK.
Joao F PassosDepartment of Physiology and Biomedical Engineering and Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA.
Gavin D RichardsonVascular Medicine and Biology Theme, Biosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, UK.
Avan A SayerAGE Research Group, Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, UK.
Newcastle University · GBMayo Clinic in Florida · USNewcastle upon Tyne Hospitals NHS Foundation Trust · GBNIHR Newcastle Biomedical Research Centre · GB

Funding

Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla, Nathan K LeBrasseur · 2019 to 2026
$28.7M
The role of sub-lethal mitochondrial apoptotic stress in cellular senescenceR01AG068048 · NIA · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2020 to 2024
$2.2M
Development of machine learning software to quantitatively map telomere induced senescence in tissue sections during agingUH3CA268103 · NCI · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2023 to 2025
$1.6M
Investigating the role of cytosolic mitochondrial double-stranded RNA in cellular senescence and agingR01AG082708 · NIA · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2023 to 2025
$1.5M
Development of machine learning software to quantitatively map telomere induced senescence in tissue sections during agingUG3CA268103 · NCI · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2021 to 2022
$1.1M
NCI NIH HHS UG3 CA268103NCI NIH HHS UH3 CA268103NIA NIH HHS P01 AG062413NIA NIH HHS R01 AG068048NIA NIH HHS R01 AG082708NIH HHS 1R01AG068048-01
6 · The paper itself

Abstract

Cellular senescence has emerged as a fundamental biological mechanism underpinning the ageing process and has been implicated in the pathogenesis of an increasing number of age-related conditions. Cellular senescence is a cell fate originally defined as an irreversible loss of replicative potential although it is now clear that it can be induced by a variety of mechanisms independent of replication and telomere attrition. The drivers include a persistent DNA damage response causing multiple alterations in cellular function. Senescent cells secrete a range of mediators that drive chronic inflammation and can convert other cells to the senescent state-the senescence-associated secretory phenotype. Much research to date has been conducted in animal models, but it is now clear that senescent cells accompany ageing in humans and their presence is an important driver of disease across systems. Proof-of-concept work suggests that preventing or reversing senescence may be a viable strategy to counteract human ageing and age-related disease. Possible interventions include exercise, nutrition and senolytics/senostatic drugs although there are a number of potential limitations to the use of senotherapeutics. These interventions are generally tested for single-organ conditions, but the real power of this approach is the potential to tackle multiple age-related conditions. The litmus test for this exciting new class of therapies, however, will be whether they can improve healthy life expectancy rather than merely extending lifespan. The outcomes measured in clinical studies need to reflect these aims if senotherapeutics are to gain the trust of clinicians, patients and the public.

Indexed as

Cellular SenescenceSenotherapeuticsAgingAnimalsHumansInflammationLongevitySenotherapeuticscellular senescencehuman ageinginterventionsolder peoplesenescence-associated secretory phenotypesenolyticssenotherapeutics

Identifiers

PMID37466640
PMCPMC10355181
OpenAlexW4384663250

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.