Evidence map›Paper›PMID 25005743›Full record

ReviewCurrent opinion in genetics & development2014

Alive and well? Exploring disease by studying lifespan.

Jamie O Brett, Thomas A Rando

Abstract readReview
In one paragraph

Review in Current opinion in genetics & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. IL-10 prevents aging-associated inflammation and insulin resistance in skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  6. Review
  7. 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

2 authors.

Jamie O BrettInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Thomas A RandoInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA; Paul F. Glenn Laboratories for the Biology of Aging, Stanford University School of Medicine, Stanford, CA, USA; Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA; Neurology Service and Rehabilitation Research and Development Center of Excellence, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA. Electronic address: rando@stanford.edu.

Funding

Wnt signaling in muscle stem cell agingP01AG036695 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARGARET A. GOODELL · 2011 to 2026
$29.3M
Stanford Training Program in Aging ResearchT32AG047126 · NIA · STANFORD UNIVERSITY · PI VYJEYANTHI S PERIYAKOIL, TONY WYSS-CORAY · 2014 to 2026
$4.3M
A New Muscle-Brain Axis Underlying the Cognitive Benefits of Physical ActivityR01AG047820 · NIA · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI RANDO, THOMAS A., WYSS-CORAY, TONY · 2013 to 2017
$3.5M
Notch Signaling and Satellite Cell ActivationR01AG023806 · NIA · STANFORD UNIVERSITY · PI RANDO, THOMAS A. · 2005 to 2009
$1.2M
NIA NIH HHS P01 AG036695NIA NIH HHS R01 AG023806NIA NIH HHS R01 AG047820NIA NIH HHS T32 AG047126
6 · The paper itself

Abstract

A common concept in aging research is that chronological age is the most important risk factor for the development of diverse diseases, including degenerative diseases and cancers. The mechanistic link between the aging process and disease pathogenesis, however, is still enigmatic. Nevertheless, measurement of lifespan, as a surrogate for biological aging, remains among the most frequently used assays in aging research. In this review, we examine the connection between 'normal aging' and age-related disease from the point of view that they form a continuum of aging phenotypes. This notion of common mechanisms gives rise to the converse postulate that diseases may be risk factors for accelerated aging. We explore the advantages and caveats associated with using lifespan as a metric to understand cell and tissue aging, focusing on the elucidation of molecular mechanisms and potential therapies for age-related diseases.

Indexed as

DiseaseAgingAnimalsGene-Environment InteractionHumansLongevityModels, BiologicalMutationPhenotypeSignal Transduction

Identifiers

PMID25005743
PMCPMC4253307

What OpenQuestion holds

Textmetadata
LicenceTDM
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.