ArticleNPJ Regenerative medicine2021
Inhibition of nuclear factor (erythroid-derived 2)-like 2 promotes hepatic progenitor cell activation and differentiation.
Article in NPJ Regenerative medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Chronic infection and metabolic stress: a converging axis driving hypertension and metabolic dysfunction-associated steatotic liver disease outcomes.American journal of hypertension · 2026Review
- Mfap4: a promising target for enhanced liver regeneration and chronic liver disease treatment.NPJ Regenerative medicine · 2023Article
- Ductular reaction in non-alcoholic fatty liver disease: When Macbeth is perverted.World journal of hepatology · 2023Review
- NRF2 and the Moirai: Life and Death Decisions on Cell Fates.Antioxidants & redox signaling · 2023Review
- Targeting NRF2 to promote epithelial repair.Biochemical Society transactions · 2023Review
- Redox-Dependent Modulation of Human Liver Progenitor Cell Line Fate.International journal of molecular sciences · 2023Article
- FoxO3 restricts liver regeneration by suppressing the proliferation of hepatocytes.NPJ Regenerative medicine · 2022Article
- Nrf2 Transcriptional Activity Governs Intestine Development.International journal of molecular sciences · 2022Article
- Ssu72-HNF4α signaling axis classify the transition from steatohepatitis to hepatocellular carcinoma.Cell death and differentiation · 2022Article
- Liver Regeneration and Cell Transplantation for End-Stage Liver Disease.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
The stem cell ability to self-renew and lead regeneration relies on the balance of complex signals in their microenvironment. The identification of modulators of hepatic progenitor cell (HPC) activation is determinant for liver regeneration and may improve cell transplantation for end-stage liver disease. This investigation used different models to point out the Nuclear factor (erythroid-derived 2)-like 2 (NRF2) as a key regulator of the HPC fate. We initially proved that in vivo models of biliary epithelial cells (BECs)/HPC activation show hepatic oxidative stress, which activates primary BECs/HPCs in vitro. NRF2 downregulation and silencing were associated with morphological, phenotypic, and functional modifications distinctive of differentiated cells. Furthermore, NRF2 activation in the biliary tract repressed the ductular reaction in injured liver. To definitely assess the importance of NRF2 in HPC biology, we applied a xenograft model by inhibiting NRF2 in the human derived HepaRG cell line and transplanting into SCID/beige mice administered with anti-Fas antibody to induce hepatocellular apoptosis; this resulted in effective human hepatocyte repopulation with reduced liver injury. To conclude, NRF2 inhibition leads to the activation and differentiation of liver progenitors. This redox-dependent transcription factor represents a potential target to regulate the commitment of undifferentiated hepatic progenitors into specific lineages.
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.