Evidence map›Paper›PMID 29543808›Full record

ArticlePLoS computational biology2018

Epigenetic regulation of cell fate reprogramming in aging and disease: A predictive computational model.

Núria Folguera-Blasco, Elisabet Cuyàs, Javier A Menéndez, Tomás Alarcón

Abstract read
In one paragraph

Article in PLoS computational biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Epigenetics, Resilience, Protective Factors and Factors Promoting Positive Outcomes: A Scoping Review.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. NETISCE: a network-based tool for cell fate reprogramming.NPJ systems biology and applications · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Aging · 2019
    Article
  15. Article
  16. Review
  17. Mitostemness.Cell cycle (Georgetown, Tex.) · 2018
    Review
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.

Núria Folguera-BlascoCentre de Recerca Matemàtica, Edifici C, Campus de Bellaterra, Bellaterra (Barcelona), Spain.ORCID 0000-0003-1584-5885
Elisabet CuyàsMolecular Oncology Group, Girona Biomedical Research Institute (IDIBGI), Girona, Spain.
Javier A MenéndezMolecular Oncology Group, Girona Biomedical Research Institute (IDIBGI), Girona, Spain.
Tomás AlarcónCentre de Recerca Matemàtica, Edifici C, Campus de Bellaterra, Bellaterra (Barcelona), Spain.ORCID 0000-0002-8566-3676

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the control of epigenetic regulation is key to explain and modify the aging process. Because histone-modifying enzymes are sensitive to shifts in availability of cofactors (e.g. metabolites), cellular epigenetic states may be tied to changing conditions associated with cofactor variability. The aim of this study is to analyse the relationships between cofactor fluctuations, epigenetic landscapes, and cell state transitions. Using Approximate Bayesian Computation, we generate an ensemble of epigenetic regulation (ER) systems whose heterogeneity reflects variability in cofactor pools used by histone modifiers. The heterogeneity of epigenetic metabolites, which operates as regulator of the kinetic parameters promoting/preventing histone modifications, stochastically drives phenotypic variability. The ensemble of ER configurations reveals the occurrence of distinct epi-states within the ensemble. Whereas resilient states maintain large epigenetic barriers refractory to reprogramming cellular identity, plastic states lower these barriers, and increase the sensitivity to reprogramming. Moreover, fine-tuning of cofactor levels redirects plastic epigenetic states to re-enter epigenetic resilience, and vice versa. Our ensemble model agrees with a model of metabolism-responsive loss of epigenetic resilience as a cellular aging mechanism. Our findings support the notion that cellular aging, and its reversal, might result from stochastic translation of metabolic inputs into resilient/plastic cell states via ER systems.

Indexed as

AgingAnimalsBayes TheoremCell DifferentiationCellular ReprogrammingCellular SenescenceChromatinComputational BiologyComputer SimulationDNA MethylationEpigenesis, GeneticForecastingHistone CodeHistonesHumansKineticsChromatinHistones

Identifiers

PMID29543808
PMCPMC5871006

What OpenQuestion holds

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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.