Evidence map›Paper›PMID 26668170›Full record

ReviewMolecular biology of the cell2015

The cell biology of aging.

Race DiLoreto, Coleen T Murphy

Open access · greenAbstract readReview
In one paragraph

Review in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

104 citing papers in PubMed, 179 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Simultaneous ManNAc and Neu5Ac Quantification in Human Sera by LC-MS/MS.International journal of molecular sciences · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Phenotypic and metabonomics studies of FMOs in C. elegans and their roles in lifespan extension.Metabolomics : Official journal of the Metabolomic Society · 2025
    Article
  10. Article
  11. Article
  12. Non-autonomy of age-related morphological changes in thebioRxiv : the preprint server for biology · 2025
    Article
  13. Review
  14. Weight of time: exploring the link between obesity and aging.Aging clinical and experimental research · 2025
    Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

44 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 1 institution in 1 country.

Race DiLoretoDepartment of Molecular Biology, Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544.
Coleen T MurphyDepartment of Molecular Biology, Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544 ctmurphy@Princeton.edu.
Princeton University · US

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007388 · NIGMS · PRINCETON UNIVERSITY · PI CRISTEA, ILEANA M. · 1985 to 2022
$27.4M
NIGMS NIH HHS T32 GM 007388NIGMS NIH HHS T32 GM007388
6 · The paper itself

Abstract

One of the original hypotheses of organismal longevity posits that aging is the natural result of entropy on the cells, tissues, and organs of the animal--a slow, inexorable slide into nonfunctionality caused by stochastic degradation of its parts. We now have evidence that aging is instead at least in part genetically regulated. Many mutations have been discovered to extend lifespan in organisms of all complexities, from yeast to mammals. The study of metazoan model organisms, such as Caenorhabditis elegans, has been instrumental in understanding the role of genetics in the cell biology of aging. Longevity mutants across the spectrum of model organisms demonstrate that rates of aging are regulated through genetic control of cellular processes. The regulation and subsequent breakdown of cellular processes represent a programmatic decision by the cell to either continue or abandon maintenance procedures with age. Our understanding of cell biological processes involved in regulating aging have been particularly informed by longevity mutants and treatments, such as reduced insulin/IGF-1 signaling and dietary restriction, which are critical in determining the distinction between causes of and responses to aging and have revealed a set of downstream targets that participate in a range of cell biological activities. Here we briefly review some of these important cellular processes.

Indexed as

AgingAnimalsCaenorhabditis elegansGene Expression RegulationHumansInsulinInsulin-Like Growth Factor ILongevityMutationSignal TransductionInsulinInsulin-Like Growth Factor I

Identifiers

PMID26668170
PMCPMC4678010
OpenAlexW2240518777

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.