Evidence map›Paper›PMID 41171586›Full record

ReviewStem cell reviews and reports2026

Liver Regeneration: Polyploidy and Cellular Senescence as Potential Regulators.

Saeedeh Zare Jalise, Sina Habibi, Zahra Khosrowpour, Abbas Piryaei, Faezeh Hosseinzadeh, Mona Navaei-Nigjeh, Leyla Fath-Bayati

Abstract readReview
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In one paragraph

Review in Stem cell reviews and reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Polyploidy: A macromutational force pushing bioeconomic developments.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Saeedeh Zare JaliseStudent Research Committee, Qom University of Medical Sciences, Qom, Iran.
Sina HabibiDepartment of Hematology and Blood Banking, Faculty of Allied Medicine, Iran University of Medical Sciences, Tehran, Iran.
Zahra KhosrowpourDepartment of Pediatrics, University of Minnesota, Minneapolis, USA.
Abbas PiryaeiDepartment of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Faezeh HosseinzadehDepartment of Tissue Engineering and Applied Cell Sciences, School of Medicine, Qom University of Medical Sciences, Qom, Iran.
Mona Navaei-NigjehPharmaceutical Sciences Research Center, The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Science, Tehran, Iran.
Leyla Fath-BayatiDepartment of Tissue Engineering and Applied Cell Sciences, School of Medicine, Qom University of Medical Sciences, Qom, Iran. lfbayati@razi.tums.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver is a highly versatile and resilient organ that is crucial for metabolism, detoxification, digestion, and immune regulation. Its remarkable regenerative capacity is driven primarily by two key cellular processes: hepatocyte polyploidy and cellular senescence. This review explores the complex roles of polyploidy, in which hepatocytes possess multiple chromosome sets, and senescence, characterized by irreversible cell cycle arrest, in maintaining liver homeostasis and facilitating regeneration. Polyploid hepatocytes increase genetic and metabolic diversity, enabling the liver to withstand stress and recover from injury through mechanisms such as compensatory regeneration, depolyploidization, and the fusion of extrinsic stem cells. Concurrently, cellular senescence acts as a protective barrier against uncontrolled cell proliferation and genomic instability while also promoting tissue repair via the senescence-associated secretory phenotype (SASP). The interplay between polyploidy and senescence is regulated by critical molecular pathways, including the Hippo, PI3K/Akt, and p53 signaling pathways, which balance cell proliferation, differentiation, and apoptosis. Additionally, this review discusses the therapeutic potential of targeting these processes to increase liver regeneration, prevent fibrosis, and reduce the risk of hepatocellular carcinoma (HCC). Emerging strategies such as senolytic drugs, stem cell therapies, and cytokine modulation offer promising avenues for treating chronic liver diseases. However, challenges remain in fully understanding the functional distinctions between diploid and polyploid hepatocytes and managing the dual roles of senescence. Future research should focus on molecular insights and targeted interventions to optimize liver health and regenerative outcomes.

Indexed as

Cellular SenescenceLiver RegenerationPolyploidyAnimalsCell ProliferationHepatocytesHumansLiverSignal TransductionCellular polyploidyCellular senescenceLiver regenerationNuclear polyploidyRegulatory

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.