Hippo Pathway Activity Influences Liver Cell Fate
Open accessAbstract
The Hippo-signaling pathway is an important regulator of cellular proliferation and organ size. However, little is known about the role of this cascade in the control of cell fate. Employing a combination of lineage tracing, clonal analysis, and organoid culture approaches, we demonstrate that Hippo pathway activity is essential for the maintenance of the differentiated hepatocyte state. Remarkably, acute inactivation of Hippo pathway signaling in vivo is sufficient to dedifferentiate, at very high efficiencies, adult hepatocytes into cells bearing progenitor characteristics. These hepatocyte-derived progenitor cells demonstrate self-renewal and engraftment capacity at the single-cell level. We also identify the NOTCH-signaling pathway as a functional important effector downstream of the Hippo transducer YAP. Our findings uncover a potent role for Hippo/YAP signaling in controlling liver cell fate and reveal an unprecedented level of phenotypic plasticity in mature hepatocytes, which has implications for the understanding and manipulation of liver regeneration.
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Following diverse injuries, often involving cholestasis, YAP signalling drives hepatocyte reprogramming via SOX9 induction.
“Following diverse injuries, often involving cholestasis, YAP signalling also drives hepatocyte reprogramming via SOX9 induction.”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [59]
The Results sections on YAP-driven reprogramming and NOTCH signaling show that activating YAP in hepatocytes induces a progenitor-like fate and upregulates Sox9. The paper does not establish that this YAP–SOX9 process occurs following diverse injuries, often involving cholestasis; its Discussion mentions cholestatic disorders as a context in which hepatocytes can express biliary markers. (LLM, conf=0.86)
Experimental — accuracy not yet measuredReprogrammed zone 1 hepatocytes exhibited reduced metabolic function, upregulated tissue stem cell markers and increased proliferative capacity, contributing to regeneration.
“These reprogrammed zone 1 hepatocytes exhibited reduced metabolic function, upregulated tissue stem cell markers and increased proliferative capacity, contributing to regeneration.59,60,100,101”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [59]
The Results sections on the liver progenitor cell program and single-hepatocyte de-differentiation report loss of hepatocyte-specific gene expression, acquisition of progenitor markers, and proliferation after YAP activation (page numbers unavailable). The paper does not identify the reprogrammed cells specifically as zone 1 hepatocytes or demonstrate reduced metabolic function. Its Discussion describes a possible role in liver repair, rather than showing that these cells contributed to regeneration. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAcute YAP overexpression results in hepatocyte reprogramming into BEC.
“Acute YAP overexpression results in hepatocyte reprogramming into BEC10.”
From HBO1 functions as an epigenetic barrier to hepatocyte plasticity and reprogramming during liver injury (2025) · cites this paper as [10]
In Results, under “YAP activation de-differentiates single adult hepatocytes” (page unavailable), lineage tracing shows that YAP induction gives hepatocytes ductal markers and a ductal/progenitor-like fate. The paper does not establish that acute overexpression converts them into mature biliary epithelial cells: many cells at one week retained a hepatocyte marker, and the reported fate change progressed over weeks. (LLM, conf=0.85)
Experimental — accuracy not yet measuredYAP is necessary and sufficient for hepatocyte reprogramming into ductal cells.
“YAP, the main transducer of the Hippo pathway, has been reported to be necessary and sufficient for hepatocyte reprogramming into ductal cells10,11.”
From HBO1 functions as an epigenetic barrier to hepatocyte plasticity and reprogramming during liver injury (2025) · cites this paper as [10]
The Results section, “YAP activation de-differentiates single adult hepatocytes” (page unavailable), explicitly says high YAP levels are sufficient to impose a ductal/progenitor-like fate on adult hepatocytes. The passages found do not establish that YAP is necessary for hepatocyte-to-ductal reprogramming; the loss-of-function result in “NOTCH signaling downstream of YAP during reprogramming” concerns NOTCH signaling, not YAP. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIncreased chromatin accessibility near YAP target genes suggests a pivotal role for YAP/TEAD signaling in the reprogramming process.
“Furthermore, increased chromatin accessibility near YAP target genes suggested a pivotal role for YAP/TEAD signaling in the reprogramming process (Figure S1C), supporting previous data10.”
From HBO1 functions as an epigenetic barrier to hepatocyte plasticity and reprogramming during liver injury (2025) · cites this paper as [10]
The Results sections on the liver progenitor program and NOTCH signaling support a role for YAP/TEAD in hepatocyte reprogramming: they report YAP-driven fate changes and YAP/TEAD binding and regulation of NOTCH-pathway genes. The paper reports chromatin occupancy, not increased chromatin accessibility near YAP target genes, so it does not support the specific observation used in the citing sentence. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Under physiological conditions, activation of YAP is necessary and sufficient to reprogram hepatocytes and to precisely control developmental outcomes, organ size and tissue repair.
“Under physiological conditions, activation of YAP is necessary and sufficient to not only reprogram hepatocytes but to precisely control developmental outcomes, organ size and tissue repair10,16,40,41.”
From HBO1 functions as an epigenetic barrier to hepatocyte plasticity and reprogramming during liver injury (2025) · cites this paper as [10]
The Results section, “YAP activation de-differentiates single adult hepatocytes” (page not supplied), reports that high levels of YAP are sufficient to impose a progenitor-like fate on adult hepatocytes. It does not establish that YAP activation is necessary for reprogramming under physiological conditions. The Discussion (page not supplied) describes a possible role in liver repair, rather than demonstrating precise control of developmental outcomes, organ size, and tissue repair. (LLM, conf=0.87)
Experimental — accuracy not yet measuredLineage-tracing studies in animal models have confirmed that hepatocytes contribute to bile duct remodeling following cholangiocyte injury.
“Lineage-tracing studies in animal models have confirmed that hepatocytes contribute to bile duct remodeling following cholangiocyte injury10,43–48”
From HBO1 functions as an epigenetic barrier to hepatocyte plasticity and reprogramming during liver injury (2025) · cites this paper as [10]
The Results (no page supplied) report lineage tracing in mice showing that hepatocytes can form ductular structures after Hippo-pathway manipulation. The Discussion also reports lineage-tracing evidence of hepatocytes acquiring biliary features during injury. Neither passage establishes that hepatocytes contribute to bile duct remodeling specifically following cholangiocyte injury. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIn periportal injury, LPLCs are mainly generated in the region 1-5 layers away from injured bile ducts.
“In periportal injury, LPLCs are mainly generated in the region 1-5 layers away from injured bile ducts.[7][8][9]12,13”
From Kupffer-cell-derived IL-6 is repurposed for hepatocyte dedifferentiation via activating progenitor genes from injury-specific enhancers (2023) · cites this paper as [12]
The Introduction (page unavailable) says oval cells emerge from bile ducts under extreme stress or chronic injury. The Results report that YAP-induced progenitor-like changes initially appear around portal areas, but this is not a measurement of periportal injury. Neither passage supports the claim that LPLCs are mainly generated 1–5 cell layers from injured bile ducts. (LLM, conf=0.78)
Experimental — accuracy not yet measuredYAP promotes SRY-box transcription factor 9 (SOX9) expression in hepatocytes and may confer the hybrid hepatocyte-biliary identity of periportal SOX9+ hepatocytes.
“However, YAP promotes SRY-box transcription factor 9 (SOX9) expression in hepatocytes59 and may confer the hybrid hepatocyte-biliary identity of periportal SOX9+ hepatocytes.60”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [59]
Hepatocytes display remarkable plasticity and under some conditions can transdifferentiate into BECs.
“Hepatocytes display remarkable plasticity and under some conditions can transdifferentiate into BECs, epithelial cells of the bile ducts with completely different morphology, gene expression and function59,[97], [98], [99]”
From Distinct hepatocyte identities in liver homeostasis and regeneration (2023) · cites this paper as [59]
Even at day 28, reprogrammed hepatocytes maintained distinct chromatin accessibility compared to BECs, despite resembling them morphologically and transcriptionally.
“Even at this later stage, reprogrammed hepatocytes maintained distinct chromatin accessibility compared to BECs (Figure 1H), despite resembling them morphologically and transcriptionally10 (Figure S1E).”
From HBO1 functions as an epigenetic barrier to hepatocyte plasticity and reprogramming during liver injury (2025) · cites this paper as [10]
Nuclear YAP1 is able to induce hepatocyte dedifferentiation into clonogenic progenitors in vivo.
“only very recent studies using a mosaic YAP1 induction model have shown that nuclear YAP1 is able to induce hepatocyte dedifferentiation into clonogenic progenitors in vivo (Yimlamai et al., 2014).”
From Hippo Signaling Influences HNF4A and FOXA2 Enhancer Switching during Hepatocyte Differentiation (2014) · cites this paper as Yimlamai et al., 2014
Further experiments in mice have shown that hepatocytes can change into a biliary ductular phenotype and later re-differentiate into hepatocytes.
“Further experiments in mice have shown that hepatocytes can change into a biliary ductular phenotype21, 22 then later re-differentiate into hepatocytes23.”
From Hepatic progenitor cells of biliary origin with liver repopulation capacity (2015) · cites this paper as [22]
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- Authors
- Yimlamai, D., Christodoulou, C., Galli, G. G., Yanger, K., Pepe-Mooney, B., Gurung, B., Shrestha, K., Cahan, P., Stanger, B. Z., & Camargo, F. D.
- Affiliations
- Boston Children's Hospital (US)
- University of Pennsylvania (US)
- Corresponding author
- Camargo, Fernando D.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2014-06
- Volume
- 157
- Issue
- 6
- Pages
- 1324-1338
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4136468
- OpenAlex
- W2028593002
- Cited by
- 857
- References
- 48
- Citations by year
- 2026: 34 · 2025: 52 · 2024: 62 · 2023: 64 · 2022: 94 · 2021: 82 · 2020: 91 · 2019: 80 · 2018: 79 · 2017: 58 · 2016: 82 · 2015: 57 · 2014: 20
- FWCI
- 36.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AR064036, DK083355, DK099559)
- American-Italian Cancer Foundation
- National Institute of Diabetes and Digestive and Kidney Diseases (5T32 DK007477-27)
- National Science Foundation (DGE1144152)
- U.S. Department of Defense (W81XWH-9)
- Harvard Stem Cell Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Keywords
- Hippo signaling pathway, YAP, hepatocyte dedifferentiation, hepatic progenitor cells, Notch signaling, phenotypic plasticity, liver regeneration, hepatocyte differentiation
- MeSH terms
- Hippo Signaling Pathway, YAP-Signaling Proteins, Animals, Liver, Phosphoproteins, Stem Cells, Signal Transduction, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Hepatocytes, Adaptor Proteins, Signal Transducing, Mice, Receptors, Notch, Cell Dedifferentiation
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