Academic Journal
Matrix stiffness may drive multi-cellular crosstalk via YAP signaling in biliary atresia liver fibrosis: a mechanistic review.
| Τίτλος: | Matrix stiffness may drive multi-cellular crosstalk via YAP signaling in biliary atresia liver fibrosis: a mechanistic review. |
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| Συγγραφείς: | Cheng, Jiwen |
| Πηγή: | Frontiers in Cell & Developmental Biology; 2026, p1-12, 12p |
| Θεματικοί όροι: | Extracellular matrix, YAP signaling proteins, Hepatic fibrosis, Bile ducts, Liver cells, Biliary atresia |
| Περίληψη: | Background: Biliary atresia (BA) is a devastating liver disease in infants. It leads to progressive cholangitis and fibrosis. In BA, the liver builds up too much extracellular matrix (ECM) and crosslinks it. That makes the tissue stiffer over time—a physical hallmark of fibrosis. Mechanistic Framework: Most of the current evidence comes from non-BA models and lab studies. Those studies hint that higher matrix stiffness might act as a mechanical trigger. It could activate YAP signaling, which then organizes pathological crosstalk among hepatocytes, cholangiocytes, and hepatic stellate cells (HSCs). Direct proof from BA tissue is still missing. Key Findings: This review looks at how matrix stiffness—through YAP-driven mechanotransduction—may drive pro-fibrotic changes in hepatocytes, cholangiocytes, and HSCs. We propose a self-reinforcing, multi-cellular pro-fibrotic network: stiff ECM turns on YAP in hepatocytes (which release inflammatory signals) and cholangiocytes (which secrete pro-fibrotic factors). Those activated HSCs then deposit and crosslink even more ECM. That raises stiffness further and locks YAP activation in all 3 cell types. Right now, this model rests mostly on indirect evidence. It needs BA-specific testing. Therapeutic Implications: We also touch on new strategies that target this mechanobiological circuit—YAP inhibitors and matrix-softening methods. Conclusion: By pulling together what we know about ECM mechanics, YAP mechanotransduction, and cell-cell crosstalk, this review points to the matrix stiffness–YAP axis as a likely key driver of BA fibrosis. It also looks like a promising treatment target. [ABSTRACT FROM AUTHOR] |
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| Βάση Δεδομένων: | Complementary Index |
| FullText | Text: Availability: 0 CustomLinks: – Url: https://resolver.ebsco.com/c/fiv2js/result?sid=EBSCO:edb&genre=article&issn=2296634X&ISBN=&volume=&issue=&date=20260715&spage=1&pages=1-12&title=Frontiers in Cell & Developmental Biology&atitle=Matrix%20stiffness%20may%20drive%20multi-cellular%20crosstalk%20via%20YAP%20signaling%20in%20biliary%20atresia%20liver%20fibrosis%3A%20a%20mechanistic%20review.&aulast=Cheng%2C%20Jiwen&id=DOI:10.3389/fcell.2026.1842681 Name: Full Text Finder (for New FTF UI) (ns324271) Category: fullText Text: Full Text Finder MouseOverText: Full Text Finder |
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| Header | DbId: edb DbLabel: Complementary Index An: 195368665 RelevancyScore: 1061 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 1060.7685546875 |
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| Items | – Name: Title Label: Title Group: Ti Data: Matrix stiffness may drive multi-cellular crosstalk via YAP signaling in biliary atresia liver fibrosis: a mechanistic review. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Cheng%2C+Jiwen%22">Cheng, Jiwen</searchLink> – Name: TitleSource Label: Source Group: Src Data: Frontiers in Cell & Developmental Biology; 2026, p1-12, 12p – Name: Subject Label: Subject Terms Group: Su Data: <searchLink fieldCode="DE" term="%22Extracellular+matrix%22">Extracellular matrix</searchLink><br /><searchLink fieldCode="DE" term="%22YAP+signaling+proteins%22">YAP signaling proteins</searchLink><br /><searchLink fieldCode="DE" term="%22Hepatic+fibrosis%22">Hepatic fibrosis</searchLink><br /><searchLink fieldCode="DE" term="%22Bile+ducts%22">Bile ducts</searchLink><br /><searchLink fieldCode="DE" term="%22Liver+cells%22">Liver cells</searchLink><br /><searchLink fieldCode="DE" term="%22Biliary+atresia%22">Biliary atresia</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Background: Biliary atresia (BA) is a devastating liver disease in infants. It leads to progressive cholangitis and fibrosis. In BA, the liver builds up too much extracellular matrix (ECM) and crosslinks it. That makes the tissue stiffer over time—a physical hallmark of fibrosis. Mechanistic Framework: Most of the current evidence comes from non-BA models and lab studies. Those studies hint that higher matrix stiffness might act as a mechanical trigger. It could activate YAP signaling, which then organizes pathological crosstalk among hepatocytes, cholangiocytes, and hepatic stellate cells (HSCs). Direct proof from BA tissue is still missing. Key Findings: This review looks at how matrix stiffness—through YAP-driven mechanotransduction—may drive pro-fibrotic changes in hepatocytes, cholangiocytes, and HSCs. We propose a self-reinforcing, multi-cellular pro-fibrotic network: stiff ECM turns on YAP in hepatocytes (which release inflammatory signals) and cholangiocytes (which secrete pro-fibrotic factors). Those activated HSCs then deposit and crosslink even more ECM. That raises stiffness further and locks YAP activation in all 3 cell types. Right now, this model rests mostly on indirect evidence. It needs BA-specific testing. Therapeutic Implications: We also touch on new strategies that target this mechanobiological circuit—YAP inhibitors and matrix-softening methods. Conclusion: By pulling together what we know about ECM mechanics, YAP mechanotransduction, and cell-cell crosstalk, this review points to the matrix stiffness–YAP axis as a likely key driver of BA fibrosis. It also looks like a promising treatment target. [ABSTRACT FROM AUTHOR] – Name: Abstract Label: Group: Ab Data: <i>Copyright of Frontiers in Cell & Developmental Biology is the property of Frontiers Media S.A. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.3389/fcell.2026.1842681 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 12 StartPage: 1 Subjects: – SubjectFull: Extracellular matrix Type: general – SubjectFull: YAP signaling proteins Type: general – SubjectFull: Hepatic fibrosis Type: general – SubjectFull: Bile ducts Type: general – SubjectFull: Liver cells Type: general – SubjectFull: Biliary atresia Type: general Titles: – TitleFull: Matrix stiffness may drive multi-cellular crosstalk via YAP signaling in biliary atresia liver fibrosis: a mechanistic review. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Cheng, Jiwen IsPartOfRelationships: – BibEntity: Dates: – D: 15 M: 07 Text: 2026 Type: published Y: 2026 Identifiers: – Type: issn-print Value: 2296634X Titles: – TitleFull: Frontiers in Cell & Developmental Biology Type: main |
| ResultId | 1 |