Evidence map›Paper›PMID 26077337›Full record

ArticleAging cell2015

Genetic evidence for common pathways in human age-related diseases.

Simon C Johnson, Xiao Dong, Jan Vijg, Yousin Suh

Abstract read
In one paragraph

Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed.

  1. Evolutionary genetics of ageing.Nature reviews. Genetics · 2026
    Review
  2. Article
  3. Ligand-specific regulation of a binary enhancer code dictating cellular senescence.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Polygenic prediction of human longevity on the supposition of pervasive pleiotropy.medRxiv : the preprint server for health sciences · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Diet andNutrients · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

4 authors.

Simon C JohnsonDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Xiao DongDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Jan VijgDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.
Yousin SuhDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI Ulrich Steidl · 1985 to 2026
$111.2M
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
(PQB4) Age-cancer interplay of genome and epi-genome in human lungR01CA180126 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI AUTON, ADAM, SPIVACK, SIMON D · 2013 to 2016
$2.8M
New Methods to Uncover Global Transcriptional Programs for Disease Risk VariantsR01GM104459 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI SUH, YOUSIN · 2013 to 2016
$2.5M
MECHANISMS OF CARDIOVASCULAR DISEASEST32HL007675 · NHLBI · YESHIVA UNIVERSITY · PI SIBINGA, NICHOLAS E · 1989 to 2013
$2.2M
NCI NIH HHS CA180126NCI NIH HHS P30 CA013330NHLBI NIH HHS 5T32HL007675-25NIA NIH HHS AG017242NIA NIH HHS P01 AG017242NIGMS NIH HHS GM104459NIGMS NIH HHS R01 GM104459
6 · The paper itself

Abstract

Aging is the single largest risk factor for chronic disease. Studies in model organisms have identified conserved pathways that modulate aging rate and the onset and progression of multiple age-related diseases, suggesting that common pathways of aging may influence age-related diseases in humans as well. To determine whether there is genetic evidence supporting the notion of common pathways underlying age-related diseases, we analyzed the genes and pathways found to be associated with five major categories of age-related disease using a total of 410 genomewide association studies (GWAS). While only a small number of genes are shared among all five disease categories, those found in at least three of the five major age-related disease categories are highly enriched for apoliprotein metabolism genes. We found that a more substantial number of gene ontology (GO) terms are shared among the 5 age-related disease categories and shared GO terms include canonical aging pathways identified in model organisms, such as nutrient-sensing signaling, translation, proteostasis, stress responses, and genome maintenance. Taking advantage of the vast amount of genetic data from the GWAS, our findings provide the first direct evidence that conserved pathways of aging simultaneously influence multiple age-related diseases in humans as has been demonstrated in model organisms.

Indexed as

Genome-Wide Association StudyAgingApolipoproteins EDiseaseHumansLongevityPolymorphism, Single NucleotideRisk FactorsApolipoproteins EageingaginggeneticsgerontogeneshumaninflammationInk4alongevity gene

Identifiers

PMID26077337
PMCPMC4568968

What Socratic 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 Socratic graph.