ArticleGenes & development2022
Centriole signaling restricts hepatocyte ploidy to maintain liver integrity.
Article in Genes & development, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- PIDDosome deficiency impairs bone remodeling by increasing osteoclast ploidy and function.Cell death and differentiation · 2026Article
- The PIDDosome controls cardiomyocyte polyploidization during postnatal heart development.Cell death and differentiation · 2026Article
- Caspase-2 deficiency drives pathogenic liver polyploidy and increases age-associated hepatocellular carcinoma in mice.Science advances · 2026Article
- Review
- Centriole structural integrity defects are a crucial feature of hydrolethalus syndrome.The Journal of cell biology · 2025Article
- Paracancerous binuclear hepatocytes assessed by computer program is a novel biomarker for short term recurrence of hepatocellular carcinoma after surgery.Scientific reports · 2025Article
- Rapid and sustained degradation of the essential centrosome protein CEP192 in live mice using the AID2 system.Science advances · 2025Article
- Caspase-2 kills cells with extra centrosomes.Science advances · 2024Article
- Integrating the Study of Polyploidy Across Organisms, Tissues, and Disease.Annual review of genetics · 2024Review
- Stepwise phosphorylation and SUMOylation of PIDD1 drive PIDDosome assembly in response to DNA repair failure.Nature communications · 2024Article
- Centrioles are frequently amplified in early B cell development but dispensable for humoral immunity.Nature communications · 2024Article
- The AID2 system offers a potent tool for rapid, reversible, or sustained degradation of essential proteins in live mice.bioRxiv : the preprint server for biology · 2024Article
- GATA binding protein 2 mediated ankyrin repeat domain containing 26 high expression in myeloid-derived cell lines.World journal of stem cells · 2024Article
- Polyploidy and mTOR signaling: a possible molecular link.Cell communication and signaling : CCS · 2024Review
- The antagonistic relationship between apoptosis and polyploidy in development and cancer.Seminars in cell & developmental biology · 2024Review
- The role of cellular polyploidy in the regeneration of the cirrhotic liver in rats and humans.Comparative cytogenetics · 2024Article
- Cellular polyploidy in organ homeostasis and regeneration.Protein & cell · 2023Article
- Endomitosis: a new cell fate in the cell cycle leading to polyploidy in megakaryocytes and hepatocytes.Journal of Zhejiang University. Science. BReview
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatocyte polyploidization is a tightly controlled process that is initiated at weaning and increases with age. The proliferation of polyploid hepatocytes in vivo is restricted by the PIDDosome-P53 axis, but how this pathway is triggered remains unclear. Given that increased hepatocyte ploidy protects against malignant transformation, the evolutionary driver that sets the upper limit for hepatocyte ploidy remains unknown. Here we show that hepatocytes accumulate centrioles during cycles of polyploidization in vivo. The presence of excess mature centrioles containing ANKRD26 was required to activate the PIDDosome in polyploid cells. As a result, mice lacking centrioles in the liver or ANKRD26 exhibited increased hepatocyte ploidy. Under normal homeostatic conditions, this increase in liver ploidy did not impact organ function. However, in response to chronic liver injury, blocking centriole-mediated ploidy control leads to a massive increase in hepatocyte polyploidization, severe liver damage, and impaired liver function. These results show that hyperpolyploidization sensitizes the liver to injury, posing a trade-off for the cancer-protective effect of increased hepatocyte ploidy. Our results may have important implications for unscheduled polyploidization that frequently occurs in human patients with 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.