ArticlebioRxiv : the preprint server for biology2026
Hepatocyte Embryonic Ectoderm Development (Eed) Deficiency Causes Liver Injury, Fibrosis, and Impacts Liver Regeneration.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
Regeneration depends on tightly coordinated transcriptional programs governed by a dynamic epigenetic landscape to regulate cell identity, proliferation, and tissue remodelling following injury. The liver is highly regenerative due to its ability to rapidly upregulate genes that drive the cell cycle and other genes important for hepatocyte proliferation. In the uninjured liver, many of these genes are poised for activation based on promoter occupancy of trimethylated histone 3 lysine 27 (H3K27me3) and regenerative stimulus provided by partial hepatectomy leads to evacuation of this mark, suggesting this is a key component of proregenerative gene regulation in the liver. H3K27me3 is deposited by the polycomb repressive complex 2 (PRC2). Were we deplete H3K27me3 using hepatocyte specific deletion of key component of PRC2, Embryonic Ectoderm Development
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