Evidence map›Paper›PMID 32978396›Full record

ArticleNature communications2020

Polyunsaturated fatty acids and p38-MAPK link metabolic reprogramming to cytoprotective gene expression during dietary restriction.

Manish Chamoli, Anita Goyala, Syed Shamsh Tabrez, Atif Ahmed Siddiqui, Anupama Singh, Adam Antebi, Gordon J Lithgow, Jennifer L Watts, Arnab Mukhopadhyay

Abstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Forward genetics ineLife · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Dietary regulation in health and disease.Signal transduction and targeted therapy · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Worms, Fat, and Death:Metabolites · 2021
    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

9 authors.

Manish Chamoli *Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.ORCID http://orcid.org/0000-0003-0339-7894
Anita Goyala *Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.
Syed Shamsh Tabrez *Molecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.
Atif Ahmed SiddiquiMolecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.
Anupama SinghMolecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.ORCID http://orcid.org/0000-0002-9311-073X
Adam AntebiDepartment of Molecular Genetics of Ageing, Max Planck Institute for Biology of Ageing, Cologne, 50931, Germany.
Gordon J LithgowBuck Institute for Research on Aging, 8001 Redwood Blvd., Novato, CA, 94945, USA.
Jennifer L WattsSchool of Molecular Biosciences, Washington State University, Pullman, WA, 99164-7520, USA.
Arnab MukhopadhyayMolecular Aging Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India. arnab@nii.ac.in.ORCID http://orcid.org/0000-0002-5266-7849

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
NIH HHS P40 OD010440
6 · The paper itself

Abstract

The metabolic state of an organism instructs gene expression modalities, leading to changes in complex life history traits, such as longevity. Dietary restriction (DR), which positively affects health and life span across species, leads to metabolic reprogramming that enhances utilisation of fatty acids for energy generation. One direct consequence of this metabolic shift is the upregulation of cytoprotective (CyTP) genes categorized in the Gene Ontology (GO) term of "Xenobiotic Detoxification Program" (XDP). How an organism senses metabolic changes during nutritional stress to alter gene expression programs is less known. Here, using a genetic model of DR, we show that the levels of polyunsaturated fatty acids (PUFAs), especially linoleic acid (LA) and eicosapentaenoic acid (EPA), are increased following DR and these PUFAs are able to activate the CyTP genes. This activation of CyTP genes is mediated by the conserved p38 mitogen-activated protein kinase (p38-MAPK) pathway. Consequently, genes of the PUFA biosynthesis and p38-MAPK pathway are required for multiple paradigms of DR-mediated longevity, suggesting conservation of mechanism. Thus, our study shows that PUFAs and p38-MAPK pathway function downstream of DR to help communicate the metabolic state of an organism to regulate expression of CyTP genes, ensuring extended life span.

Indexed as

Gene Expression RegulationAnimalsBiochemical PhenomenaCaenorhabditis elegansCaenorhabditis elegans ProteinsEicosapentaenoic AcidFatty Acids, UnsaturatedGene Knockdown TechniquesLinoleic AcidLongevityMetabolic Networks and Pathwaysp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesCaenorhabditis elegans Proteinsdrl-1 protein, C elegansEicosapentaenoic Acideicosapentaenoic acid ethyl esterFatty Acids, UnsaturatedLinoleic Acidp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine Kinases

Identifiers

PMID32978396
PMCPMC7519657

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Registered trials

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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.