Evidence map›Paper›PMID 42649478›Full record

ArticleAging cell2026

Timing-Dependent Clearance of p16-Positive Cells Mitigates Radiation-Induced Accelerated Aging.

Karla Valdivieso, Melanie Weigand, Daniela G Costa, Gung Lee, Nick Pirius, Helene Martini, Shivangi Oberai, Christina Inman, Yi Zhu, Thomas von Zglinicki and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Karla ValdiviesoDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0002-8058-5453
Melanie WeigandDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
Daniela G CostaDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0002-3795-1649
Gung LeeDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
Nick PiriusDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
Helene MartiniDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0001-8789-4585
Shivangi OberaiMolecular Pharmacology and Experimental Therapeutics Graduate Program, Mayo Clinic Graduate School of Biomedical Sciences, Rochester, Minnesota, USA.
Christina InmanDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
Yi ZhuDepartment of Cellular and Integrative Physiology, UT Health San Antonio, San Antonio, Texas, USA.ORCID https://orcid.org/0000-0002-3876-3156
Thomas von ZglinickiBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Sundeep KhoslaDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0002-2936-4372
Nathan LeBrasseurDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0002-2002-0418
João F PassosDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0001-8765-1890
Tamara TchkoniaCenter for Advanced Gerotherapeutics, Department of Medicine, Cedars-Sinai Health Sciences University, Los Angeles, California, USA.ORCID https://orcid.org/0000-0003-4623-7145
James L KirklandCenter for Advanced Gerotherapeutics, Department of Medicine, Cedars-Sinai Health Sciences University, Los Angeles, California, USA.ORCID https://orcid.org/0000-0003-1676-4905
Diana JurkDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.ORCID https://orcid.org/0000-0003-4486-0857

Funding

Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla, Nathan K LeBrasseur · 2019 to 2026
$28.7M
Effect of Aging on Preadipocyte DifferentiationR37AG013925 · NIA · MAYO CLINIC ROCHESTER · PI KIRKLAND, JAMES L. · 2016 to 2025
$6.6M
Translational Geroscience NetworkR33AG061456 · NIA · MAYO CLINIC ROCHESTER · PI JAMES L. KIRKLAND, STEPHEN B. KRITCHEVSKY · 2019 to 2026
$6.2M
The role of sub-lethal mitochondrial apoptotic stress in cellular senescenceR01AG068048 · NIA · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2020 to 2024
$2.2M
Does obesity exacerbate age-related cognitive decline via senescence?R01AG068182 · NIA · MAYO CLINIC ROCHESTER · PI JURK, DIANA · 2020 to 2024
$2.0M
Characterization of senescent cell populations in skeletal agingR01AG086085 · NIA · MAYO CLINIC ROCHESTER · PI Sundeep Khosla, David G Monroe · 2024 to 2026
$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
Investigating the Role of Adipose Senescent Cells in Cognitive Function and Alzheimer's Disease ProgressionR01AG087387 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Yi Zhu · 2024 to 2026
$1.5M
AFAR/HevolutionConnor FundGlenn Foundation for Medical ResearchHevolution HF-GRO-23-1199262-27Hevolution HR-GRO-23-1199144-8NIA NIH HHS P01 AG062413NIA NIH HHS P01AG062413NIA NIH HHS R01 AG068048NIA NIH HHS R01AG068048NIA NIH HHS R01 AG068182NIA NIH HHS R01AG068182NIA NIH HHS R01 AG082708NIA NIH HHS R01 AG086085NIA NIH HHS R01AG086085NIA NIH HHS R01 AG087387NIA NIH HHS R01AG82708NIA NIH HHS R33 AG061456NIA NIH HHS R37 AG013925NIH HHS R01AG087387NIH HHS R33AG061456NIH HHS R37AG13925NIH HHS UG3/UH3CA268103Noaber FoundationRobert and Arlene Kogod Center on AgingRobert J. and Theresa W. Ryan
6 · The paper itself

Abstract

Genotoxic stress induced by cancer therapies is increasingly recognized as a driver of accelerated aging in long-term cancer survivors, yet the mechanisms responsible for the emergence of age-related dysfunction months to years after treatment remain poorly understood. Here, we use sublethal whole-body irradiation as a model of systemic genotoxic stress to test whether senescent cells contribute to the progression of post-therapy age-related dysfunction and whether the benefits of senescent cell clearance depend on the timing of intervention. Using the INK-ATTAC mouse model, we selectively eliminated p16

Indexed as

AgingCellular SenescenceCyclin-Dependent Kinase Inhibitor p16AnimalsDNA DamageFemaleMaleMiceTime FactorsWhole-Body IrradiationCyclin-Dependent Kinase Inhibitor p16agingBBBbraincognitionirradiationsenescencesenolytictherapy induced senescence

Identifiers

PMID42649478
PMCPMC13519039

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.