Evidence map›Paper›PMID 38918603›Full record

ArticleNature aging2024

Aging promotes metabolic dysfunction-associated steatotic liver disease by inducing ferroptotic stress.

Kuo Du, Liuyang Wang, Ji Hye Jun, Rajesh K Dutta, Raquel Maeso-Díaz, Seh Hoon Oh, Dennis C Ko, Anna Mae Diehl

Abstract read
In one paragraph

Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed.

  1. Article
  2. Article
  3. Ferroptosis in liver biology and diseases.Hepatology communications · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Redefining senescence through hepatocyte fate changes in liver diseases.Trends in endocrinology and metabolism: TEM · 2026
    Review
  19. p21Nature aging · 2026
    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

8 authors.

Kuo Du *Department of Medicine, Duke University, Durham, NC, USA.
Liuyang Wang *Department of Molecular Genetics and Microbiology, Duke University, Durham, NC, USA.
Ji Hye Jun *Department of Medicine, Duke University, Durham, NC, USA.ORCID http://orcid.org/0000-0001-5716-8128
Rajesh K DuttaDepartment of Medicine, Duke University, Durham, NC, USA.
Raquel Maeso-DíazDepartment of Medicine, Duke University, Durham, NC, USA.
Seh Hoon OhDepartment of Medicine, Duke University, Durham, NC, USA.
Dennis C KoDepartment of Molecular Genetics and Microbiology, Duke University, Durham, NC, USA.
Anna Mae DiehlDepartment of Medicine, Duke University, Durham, NC, USA. annamae.diehl@duke.edu.ORCID http://orcid.org/0000-0003-1859-089X

Funding

TNF ALPHA AND RECOVERY FROM ALCOHOLIC LIVER INJURYR01AA010154 · NIAAA · JOHNS HOPKINS UNIVERSITY · PI ANNA MAE ELIZABETH DIEHL, Auinash Kalsotra · 1994 to 2026
$6.1M
Hedgehog Signaling and Adult Liver RegenerationR01DK077794 · NIDDK · DUKE UNIVERSITY · PI DIEHL, ANNA MAE ELIZABETH · 2008 to 2020
$4.6M
Hepatic Lipotoxicity, Metabolic Homeostasis and NAFLD PathogenesisR56DK134334 · NIDDK · DUKE UNIVERSITY · PI DIEHL, ANNA MAE ELIZABETH · 2023 to 2023
$493k
Targeting Hepatocyte Senescence to Improve NAFLDK01DK135793 · NIDDK · DUKE UNIVERSITY · PI Kuo Du · 2024 to 2026
$433k
American Association for the Study of Liver Diseases (AASLD) 2021 AASLD Pinnacle AwardNIAAA NIH HHS R01 AA010154NIDDK NIH HHS K01 DK135793NIDDK NIH HHS R01 DK077794NIDDK NIH HHS R56 DK134334
6 · The paper itself

Abstract

Susceptibility to the biological consequences of aging varies among organs and individuals. We analyzed hepatocyte transcriptomes of healthy young and aged male mice to generate an aging hepatocyte gene signature, used it to deconvolute transcriptomic data from humans and mice with metabolic dysfunction-associated liver disease, validated findings with functional studies in mice and applied the signature to transcriptomic data from other organs to determine whether aging-sensitive degenerative mechanisms are conserved. We discovered that the signature enriches in diseased livers in parallel with degeneration. It is also enriched in failing human hearts, diseased kidneys and pancreatic islets from individuals with diabetes. The signature includes genes that control ferroptosis. Aged mice develop more hepatocyte ferroptosis and liver degeneration than young mice when fed diets that induce metabolic stress. Inhibiting ferroptosis shifts the liver transcriptome of old mice toward that of young mice and reverses aging-exacerbated liver damage, identifying ferroptosis as a tractable, conserved mechanism for aging-related tissue degeneration.

Indexed as

AgingFerroptosisAnimalsDisease Models, AnimalFatty LiverHepatocytesHumansLiverMaleMiceMice, Inbred C57BLStress, PhysiologicalTranscriptome

Identifiers

PMID38918603
PMCPMC12810195

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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.