Evidence map›Paper›PMID 22617385›Full record

ReviewCell cycle (Georgetown, Tex.)2012

Heterochronic parabiosis for the study of the effects of aging on stem cells and their niches.

Irina M Conboy, Thomas A Rando

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

139 citing papers in PubMed, 232 citations in OpenAlex.

  1. Trial
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  11. Immunosenescence: signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025
    Review
  12. Review
  13. Hallmarks of stem cell aging.Cell stem cell · 2025
    Review
  14. Article
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  16. Review
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  18. Article
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79 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

2 authors at 2 institutions in 1 country.

Irina M ConboyDepartment of Bioengineering, University of California, Berkeley, Berkeley, CA, USA. iconboy@berkeley.edu
Thomas A Rando
Rehabilitation Research and Development Service · USUniversity of California, Berkeley · US

Funding

Wnt signaling in muscle stem cell agingP01AG036695 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARGARET A. GOODELL · 2011 to 2026
$29.3M
NIH Director's Pioneer Award (RMI)DP1OD000392 · OD · STANFORD UNIVERSITY · PI RANDO, THOMAS A. · 2005 to 2009
$3.3M
Notch Signaling and Satellite Cell ActivationR37AG023806 · NIA · STANFORD UNIVERSITY · PI RANDO, THOMAS A. · 2010 to 2019
$2.9M
Molecular Regulation of Myogenic DifferentiationR01AR056849 · NIAMS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI RANDO, THOMAS A. · 2009 to 2013
$1.5M
The Function and Regulation of Pax3 in Muscle Stem CellsR01AR062185 · NIAMS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI RANDO, THOMAS A. · 2011 to 2015
$1.5M
Notch Signaling and Satellite Cell ActivationR01AG023806 · NIA · STANFORD UNIVERSITY · PI RANDO, THOMAS A. · 2005 to 2009
$1.2M
NIAMS NIH HHS R01 AR056849NIAMS NIH HHS R01 AR062185NIA NIH HHS P01 AG036695NIA NIH HHS R01 AG023806NIA NIH HHS R01 AG 0277252NIA NIH HHS R37 AG023806NIH HHS DP1 OD000392
6 · The paper itself

Abstract

Aging is unmistakable and undeniable in mammals. Interestingly, mice develop cataracts, muscle atrophy, osteoporosis, obesity, diabetes and cognitive deficits after just 2-3 postnatal years, while it takes seven or more decades for the same age-specific phenotypes to develop in humans. Thus, chronological age corresponds differently with biological age in metazoan species and although many theories exist, we do not understand what controls the rate of mammalian aging. One interesting idea is that species-specific rate of aging represents a ratio of tissue attrition to tissue regeneration. Furthermore, current findings suggest that the age-imposed biochemical changes in the niches of tissue stem cells inhibit performance of this regenerative pool, which leads to the decline of tissue maintenance and repair. If true, slowing down stem cell and niche aging, thereby promoting tissue regeneration, could slow down the process of tissue and organismal aging. In this regard, recent studies of heterochronic parabiosis provide important clues as to the mechanisms of stem cell aging and suggest novel strategies for enhancing tissue repair in the old. Here we review current literature on the relationship between the vigor of tissue stem cells and the process of aging, with an emphasis on the rejuvenation of old tissues by the extrinsic modifications of stem cell niches.

Indexed as

Cellular SenescenceParabiosisAnimalsHumansMuscle, SkeletalRegenerationRejuvenationSignal TransductionStem Cell NicheStem CellsTransforming Growth Factor betaWnt ProteinsTransforming Growth Factor betaWnt Proteins

Identifiers

PMID22617385
PMCPMC3383588
OpenAlexW1978269248

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.