Tier 3 — preclinical

Betaine-driven Keap1 methylation promotes p62-mediated autophagy and Nrf2 stabilization to alleviate glutathione-dependent redox dyshomeostasis in liver injury

Moon Han Chang, Chae Hwan Lee, Yeongrae Cho, Ryeo Gang Son, Seoyoon Lee, Shinwoo Park, Jaeryeong Kim, Young Ho Koh, Art E Cho, Seung Pil Pack, Minseok Seo, Jin Hyup Lee, Hanvit Cha
Molecular biomedicine 2026 7(1):172

Bibliography

PubMed
PMID 42747681
PubMed Central
PMC13582688
Funding
Reported funding/support: http://dx.doi.org/10.13039/501100003725National Research Foundation of KoreaRS-2021-NR060107 http://dx.doi.org/10.13039/501100003725National Research Foundation of KoreaRS-2026-25494026 http://dx.doi.org/10.13039/501100003725National Research Foundation of KoreaRS-2025-00559195
Competing interests
Reported disclosure: Declarations. Ethics approval and consent to participate: The animal facilities and protocols were approved by the Animal Care and Use Committee of Korea University (KUIACUC-2023–0014). All animal care and experimental procedures were conducted in accordance with the Guide for the Care and Use of Laboratory Animals (National Institutes of Health). Consent for publication: Not applicable. Competing interests: The authors declare that they have no relevant financial or non-financial interests to disclose.

Study snapshot

DesignExperimental animal and/or laboratory research
ModelMouse liver-injury models, hepatocytes and human transcriptomic context
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionBetaine in biochemical/cell assays and toxic/dietary injury models
DurationModel-specific experimental regimens
EndpointsKeap1/Nrf2; Autophagy; Liver injury

What the study showed, in plain terms

Published in 2026, this source examined preclinical aging, brain and metabolic mechanisms. Design: Experimental animal and/or laboratory research. Sample/model: Experiment-specific biological replicates and model groups; see original methods. The exposure or intervention was Betaine in biochemical/cell assays and toxic/dietary injury models. Follow-up or treatment period: Model-specific experimental regimens.

The study linked betaine exposure to Keap1 modification, autophagy, Nrf2 stabilization and improved redox measures in experimental liver injury.

Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.

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Key findings

  • The study linked betaine exposure to Keap1 modification, autophagy, Nrf2 stabilization and improved redox measures in experimental liver injury.
  • The recorded outcome domains were Keap1/Nrf2; Autophagy; Liver injury.
  • The result applies to the tested exposure: Betaine in biochemical/cell assays and toxic/dietary injury models; Model-specific experimental regimens.

What this study can and cannot tell us

  • Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.
  • Cell concentrations, species, disease models and experimental routes cannot be converted directly into an effective or safe oral human regimen.
  • Source basis: Accessible full-text extract plus indexed bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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