ArticleThe American journal of pathology2019
Polyploid Hepatocytes Facilitate Adaptation and Regeneration to Chronic Liver Injury.
Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
- Quantitative assessment of liver regenerative potential during accelerated aging: regenerative reserve and regenerative status indices.Biogerontology · 2026Article
- Article
- Growth under pressure: The pros and cons of polyploidy induced by stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Review
- Generation of tetraploid organs in mice.Zoological research · 2026Article
- Diploid hepatocytes resist acetaminophen-induced liver injury through suppressed JNK signaling.Cell death & disease · 2026Article
- Distinct p21 dynamics drive alternative routes to whole-genome duplication through a common CDK4/6-dependent polyploid G0 state.bioRxiv : the preprint server for biology · 2026Article
- Liver Regeneration: Polyploidy and Cellular Senescence as Potential Regulators.Stem cell reviews and reports · 2026Review
- Role of mitogens in normal and pathological liver regeneration.Hepatology communications · 2025Review
- Heterogeneity of hepatocyte dynamics restores liver architecture after chemical, physical or viral damage.Nature communications · 2024Article
- Wounding increases nuclear ploidy in wound-proximal epidermal cells of themicroPublication biology · 2024Article
- The Ploidy State as a Determinant of Hepatocyte Proliferation.Seminars in liver disease · 2023Review
- The consequences of tetraploidy on Caenorhabditis elegans physiology and sensitivity to chemotherapeutics.Scientific reports · 2023Article
- Cellular polyploidy in organ homeostasis and regeneration.Protein & cell · 2023Article
- Effect of Hepatic Pathology on Liver Regeneration: The Main Metabolic Mechanisms Causing Impaired Hepatic Regeneration.International journal of molecular sciences · 2023Review
- Article
- Splicing factor SRSF1 deficiency in the liver triggers NASH-like pathology and cell death.Nature communications · 2023Article
- IL6 supports long-term expansion of hepatocytes in vitro.Nature communications · 2022Article
- Implications of Polyploidy and Ploidy Alterations in Hepatocytes in Liver Injuries and Cancers.International journal of molecular sciences · 2022Review
- Centriole signaling restricts hepatocyte ploidy to maintain liver integrity.Genes & development · 2022Article
- Wnt signaling regulates hepatocyte cell division by a transcriptional repressor cascade.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The liver contains diploid and polyploid hepatocytes (tetraploid, octaploid, etc.), with polyploids comprising ≥90% of the hepatocyte population in adult mice. Polyploid hepatocytes form multipolar spindles in mitosis, which lead to chromosome gains/losses and random aneuploidy. The effect of aneuploidy on liver function is unclear, and the degree of liver aneuploidy is debated, with reports showing aneuploidy affects 5% to 60% of hepatocytes. To study relationships among liver polyploidy, aneuploidy, and adaptation, mice lacking E2f7 and E2f8 in the liver (LKO), which have a polyploidization defect, were used. Polyploids were reduced fourfold in LKO livers, and LKO hepatocytes remained predominantly diploid after extensive proliferation. Moreover, nearly all LKO hepatocytes were euploid compared with control hepatocytes, suggesting polyploid hepatocytes are required for production of aneuploid progeny. To determine whether reduced polyploidy impairs adaptation, LKO mice were bred onto a tyrosinemia background, a disease model whereby the liver can develop disease-resistant, regenerative nodules. Although tyrosinemic LKO mice were more susceptible to morbidities and death associated with tyrosinemia-induced liver failure, they developed regenerating nodules similar to control mice. Analyses revealed that nodules in the tyrosinemic livers were generated by aneuploidy and inactivating mutations. In summary, we identified new roles for polyploid hepatocytes and demonstrated that they are required for the formation of aneuploid progeny and can facilitate adaptation to chronic liver disease.
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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.