ArticleNPJ Regenerative medicine2022
DNA methylation maintenance at the p53 locus initiates biliary-mediated liver regeneration.
Article in NPJ Regenerative medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Enolase 2-mediated lactylation-dependent disruption of the GNL3-MDM2-p53 axis in age-related osteoarthritis.Cellular & molecular biology letters · 2026Article
- Review
- Khdrbs1 drives re-differentiation of bipotential progenitor cells by inhibiting p53 in zebrafish biliary-mediated liver regeneration.Development (Cambridge, England) · 2025Article
- Using different zebrafish models to explore liver regeneration.Frontiers in cell and developmental biology · 2024Review
- Arouse potential stemness: Intrinsic and acquired stem cell therapeutic strategies for advanced liver diseases.Cell insight · 2023Review
- The MRN complex maintains the biliary-derived hepatocytes in liver regeneration through ATR-Chk1 pathway.NPJ Regenerative medicine · 2023Article
- Update on Hepatobiliary Plasticity.Seminars in liver disease · 2023Article
- DNA methylation in cell plasticity and malignant transformation in liver diseases.Pharmacology & therapeutics · 2023Review
- Dedifferentiation andMolecular medicine reports · 2022Review
- Overexpression of miR-125a-5p Inhibits Hepatocyte Proliferation through the STAT3 Regulation In Vivo and In Vitro.International journal of molecular sciences · 2022Article
- C-phycocyanin alleviated cisplatin-induced oxidative stress and inflammationFrontiers in nutrition · 2022Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In cases of extensive liver injury, biliary epithelial cells (BECs) dedifferentiate into bipotential progenitor cells (BPPCs), then redifferentiate into hepatocytes and BECs to accomplish liver regeneration. Whether epigenetic regulations, particularly DNA methylation maintenance enzymes, play a role in this biliary-mediated liver regeneration remains unknown. Here we show that in response to extensive hepatocyte damages, expression of dnmt1 is upregulated in BECs to methylate DNA at the p53 locus, which represses p53 transcription, and in turn, derepresses mTORC1 signaling to activate BEC dedifferentiation. After BEC dedifferentiation and BPPC formation, DNA methylation at the p53 locus maintains in BPPCs to continue blocking p53 transcription, which derepresses Bmp signaling to induce BPPC redifferentiation. Thus, this study reveals promotive roles and mechanisms of DNA methylation at the p53 locus in both dedifferentiation and redifferentiation stages of biliary-mediated liver regeneration, implicating DNA methylation and p53 as potential targets to stimulate regeneration after extensive liver injury.
Identifiers
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Registered trials
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.