ArticleCellular and molecular gastroenterology and hepatology2025
An Nrf2-NF-κB Crosstalk Controls Hepatocyte Proliferation in the Normal and Injured Liver.
Article in Cellular and molecular gastroenterology and hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Timeless and Stainless Alcohol: Concentric Waves from Its Oxidative Metabolism and Related Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- Theaflavins counteract free fatty acid-driven oxidative-inflammatory injury in endothelial cells through Nrf2-NF-κB axis.Frontiers in immunology · 2026Article
- Article
- Lead induces cell-autonomous proliferation and metabolic reprogramming of hepatocytes.Cell death & disease · 2025Article
- Tungsten disulfide atomic crystals with RONS scavenging and liver targeting capabilities for acetaminophen-induced acute liver injury therapy.Journal of nanobiotechnology · 2025Article
- 6-Antioxidants (Basel, Switzerland) · 2025Article
- New Insights and Open Questions on the Molecular and Cellular Crosstalk Governing Hepatocyte Proliferation.Cellular and molecular gastroenterology and hepatology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsThe liver has remarkable regenerative and detoxification capacities, which require the Nrf2 and NF-κB transcription factors. Although their individual functions in hepatocytes are well characterized, knowledge about their crosstalk in the adult liver is limited.
methodsWe performed AAV8-Cre inducible, hepatocyte-specific knockout of Nrf2, the NF-κB subunit p65, or both genes to determine the individual and combined roles of these transcription factors in the intact liver of male adult mice and after acute CCl
resultsLoss of p65 alone or p65 in combination with Nrf2 caused spontaneous liver inflammation and necrosis. Gene expression profiling identified individual and common target genes of both transcription factors, including genes involved in the control of cell proliferation. Consistent with the expression of these genes, hepatocyte proliferation was reduced by Nrf2 deficiency under homeostatic conditions and after CCl
conclusionsThese results reveal a crosstalk between Nrf2 and p65 in the control of hepatocyte proliferation and point to a key role of macrophages in this effect.
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