Evidence map›Paper›PMID 35363946›Full record

ArticleAging cell2022

Targeted clearance of p21- but not p16-positive senescent cells prevents radiation-induced osteoporosis and increased marrow adiposity.

Abhishek Chandra, Anthony B Lagnado, Joshua N Farr, Madison Doolittle, Tamara Tchkonia, James L Kirkland, Nathan K LeBrasseur, Paul D Robbins, Laura J Niedernhofer, Yuji Ikeno and 4 more

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
11.0field-weighted citation impact, top 1% 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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

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  19. DEL-1 is an Endogenous Senolytic Protein that Inhibits Senescence-Associated Bone Loss.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  20. Review

34 more citing papers are in PubMed but not listed here.

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

14 authors at 3 institutions in 1 country.

Abhishek ChandraDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
Anthony B LagnadoDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
Joshua N FarrDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
Madison DoolittleRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA.
Tamara TchkoniaDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
James L KirklandDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
Nathan K LeBrasseurRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA.ORCID 0000-0002-2002-0418
Paul D RobbinsInstitute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, Minnesota, USA.ORCID 0000-0003-1068-7099
Laura J NiedernhoferInstitute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, Minnesota, USA.ORCID 0000-0002-1074-1385
Yuji IkenoDepartment of Pathology and Laboratory Medicine, University of Texas Health Science Center, San Antonio, Texas, USA.
João F PassosDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.
David G MonroeRobert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA.
Robert J PignoloDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.ORCID 0000-0002-8533-9438
Sundeep KhoslaDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA.ORCID 0000-0002-2936-4372
Mayo Clinic · USUniversity of Minnesota · USThe University of Texas Health Science Center at San Antonio · US

Funding

Mayo Clinic Center for Clinical and Translational Science (CCaTS UL1 Supplement - Dr. Timothy Curry)UL1TR002377 · NCATS · MAYO CLINIC ROCHESTER · PI VESNA D GAROVIC · 2017 to 2026
$78.4M
Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
TRANSGENIC COREP30AG013319 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI PETER J HORNSBY · 1995 to 2026
$30.6M
Targeting Cellular Senescence to Extend HealthspanP01AG062413 · NIA · MAYO CLINIC ROCHESTER · PI Nathan K LeBrasseur · 2019 to 2026
$28.7M
Validation and characterization of the identified variants associated with human longevity in mouse modelsU19AG056278 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI NIR J BARZILAI, Paul D. Robbins · 2017 to 2026
$24.5M
Using the senolytic fisetin to suppress mortality in aged mice acutely exposed to murine beta-coronavirusR01AG063543 · NIA · UNIVERSITY OF MINNESOTA · PI NIEDERNHOFER, LAURA JANE · 2019 to 2023
$3.4M
The role of sub-lethal mitochondrial apoptotic stress in cellular senescenceR01AG068048 · NIA · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2020 to 2024
$2.2M
Targeting Cellular Senescence and RAGE in Type 2 DiabetesR01DK128552 · NIDDK · UNIVERSITY OF ARIZONA · PI FARR, JOSHUA NICHOLAS · 2021 to 2025
$2.0M
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
The Role of miR-219a-5p in Bone MetabolismR01AG063707 · NIA · MAYO CLINIC ROCHESTER · PI MONROE, DAVID G · 2020 to 2024
$1.5M
Postdoctoral Training Program for Research on AgingT32AG049672 · NIA · MAYO CLINIC ROCHESTER · PI PASSOS, JOAO · 2016 to 2022
$1.3M
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
NCATS NIH HHS UL1 TR000135NCATS NIH HHS UL1 TR002377NCI NIH HHS UG3 CA268103NCI NIH HHS UH3 CA268103NIAMS NIH HHS K01 AR070241NIA NIH HHS P01 AG062413NIA NIH HHS P30 AG013319NIA NIH HHS R01 AG063543NIA NIH HHS R01 AG063707NIA NIH HHS R01 AG068048NIA NIH HHS T32 AG049672NIA NIH HHS U19 AG056278NIDDK NIH HHS R01 DK128552
6 · The paper itself

Abstract

Cellular senescence, which is a major cause of tissue dysfunction with aging and multiple other conditions, is known to be triggered by p16

Indexed as

Cyclin-Dependent Kinase Inhibitor p16OsteoporosisAdiposityAnimalsBone MarrowCellular SenescenceCyclin-Dependent Kinase Inhibitor p21MiceObesityCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21boneradiationsenescence

Identifiers

PMID35363946
PMCPMC9124310
OpenAlexW4220697696

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.