Evidence map›Paper›PMID 35902645›Full record

ArticleNature metabolism2022

Systemic induction of senescence in young mice after single heterochronic blood exchange.

Ok Hee Jeon, Melod Mehdipour, Tae-Hwan Gil, Minha Kang, Nicholas W Aguirre, Zachery R Robinson, Cameron Kato, Jessy Etienne, Hyo Gyeong Lee, Fatouma Alimirah and 5 more

Open access · greenAbstract read
In one paragraph

Article in Nature metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
11.2field-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

77 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
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  8. Article
  9. Review
  10. Research progress on blood therapy for anti-aging.Journal of advanced research · 2026
    Review
  11. Article
  12. Article
  13. Parabiosis, Assembloids, Organoids (PAO).Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

17 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

15 authors at 4 institutions in 3 countries.

Ok Hee JeonBuck Institute for Research on Aging, Novato, CA, USA. ojeon@korea.ac.kr.ORCID http://orcid.org/0000-0002-3725-7526
Melod MehdipourDepartment of Bioengineering and QB3 Institute, University of California, Berkeley, CA, USA.
Tae-Hwan GilDepartment of Biomedical Sciences, Korea University College of Medicine, Seoul, Republic of Korea.
Minha KangDepartment of Biomedical Sciences, Korea University College of Medicine, Seoul, Republic of Korea.
Nicholas W AguirreBuck Institute for Research on Aging, Novato, CA, USA.
Zachery R RobinsonDepartment of Bioengineering and QB3 Institute, University of California, Berkeley, CA, USA.
Cameron KatoDepartment of Bioengineering and QB3 Institute, University of California, Berkeley, CA, USA.ORCID http://orcid.org/0000-0002-8120-9345
Jessy EtienneDepartment of Bioengineering and QB3 Institute, University of California, Berkeley, CA, USA.ORCID http://orcid.org/0000-0003-2173-6191
Hyo Gyeong LeeDepartment of Biomedical Sciences, Korea University College of Medicine, Seoul, Republic of Korea.
Fatouma AlimirahBuck Institute for Research on Aging, Novato, CA, USA.
Vighnesh WalavalkarSurgical Pathology, University of California, San Francisco, CA, USA.
Pierre-Yves DesprezBuck Institute for Research on Aging, Novato, CA, USA.
Michael J ConboyDepartment of Bioengineering and QB3 Institute, University of California, Berkeley, CA, USA.ORCID http://orcid.org/0000-0002-6434-4772
Judith CampisiBuck Institute for Research on Aging, Novato, CA, USA. jcampisi@buckinstitute.org.ORCID http://orcid.org/0000-0001-6858-9462
Irina M ConboyDepartment of Bioengineering and QB3 Institute, University of California, Berkeley, CA, USA. iconboy@berkeley.edu.
QB3 · USBuck Institute for Research on Aging · USKorea University · KRUniversity of California, San Francisco · US

Funding

THE IMPACT OF CELLULAR DEFENSE ON THE ROLE OF Ku80 IN GENOME MAINTENANCE AND LONGP01AG017242 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 1999 to 2023
$46.1M
Cellular Senescence, astrocytes and Alzheimer's diseaseR01AG051729 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI CAMPISI, JUDITH · 2016 to 2020
$2.7M
Identifying signatures of brain aging through heterochronic blood exchangeR01AG071787 · NIA · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI MESSERSMITH, PHILLIP B, MOURRAIN, PHILIPPE · 2021 to 2025
$2.3M
New Generation Blood Exchange Devices for Enhancing Tissue Regeneration and HealthR01HL139605 · NHLBI · UNIVERSITY OF CALIFORNIA BERKELEY · PI ARAN, KIANA, CONBOY, IRINA M · 2018 to 2021
$1.6M
Treatment of Duchenne Muscular Dystrophy with Cas9 Protein Complexed to Gold NanoparticlesR01EB023776 · NIBIB · UNIVERSITY OF CALIFORNIA BERKELEY · PI CONBOY, IRINA M, MURTHY, NIREN · 2017 to 2020
$1.4M
Senescent cells as a source of pro-geronic factorsR56AG052988 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI CAMPISI, JUDITH · 2016 to 2016
$466k
Defined pharmacology for multi-tissue rejuvenation acting through youthful normalization of p16R56AG058819 · NIA · UNIVERSITY OF CALIFORNIA BERKELEY · PI CONBOY, IRINA M · 2018 to 2018
$381k
NHLBI NIH HHS R01 HL139605NIA NIH HHS P01 AG017242NIA NIH HHS R01 AG051729NIA NIH HHS R01 AG071787NIA NIH HHS R56 AG052988NIA NIH HHS R56 AG058819NIBIB NIH HHS R01 EB023776
6 · The paper itself

Abstract

abstactAgeing is the largest risk factor for many chronic diseases. Studies of heterochronic parabiosis, substantiated by blood exchange and old plasma dilution, show that old-age-related factors are systemically propagated and have pro-geronic effects in young mice. However, the underlying mechanisms how bloodborne factors promote ageing remain largely unknown. Here, using heterochronic blood exchange in male mice, we show that aged mouse blood induces cell and tissue senescence in young animals after one single exchange. This induction of senescence is abrogated if old animals are treated with senolytic drugs before blood exchange, therefore attenuating the pro-geronic influence of old blood on young mice. Hence, cellular senescence is neither simply a response to stress and damage that increases with age, nor a chronological cell-intrinsic phenomenon. Instead, senescence quickly and robustly spreads to young mice from old blood. Clearing senescence cells that accumulate with age rejuvenates old circulating blood and improves the health of multiple tissues.

Indexed as

Cellular SenescenceParabiosisAgingAnimalsMaleMice

Identifiers

PMID35902645
PMCPMC9945470
OpenAlexW4288427183

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.