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Unraveling key molecules mediating the mechanisms of YAP deletion or inhibition in liver fibrosis regression through a multi-omics approach

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dc.contributor.authorShihui Liu
dc.contributor.authorHejing Ruan
dc.contributor.authorYuzhe Cheng
dc.contributor.authorYan Qiao
dc.contributor.authorJiawei Wang
dc.contributor.authorXiaojun Liu
dc.contributor.authorChuanmiao Liu
dc.contributor.authorWen Zhao
dc.contributor.authorSiyuan Wang
dc.contributor.departmentBiologĂ­a Celular e HistologĂ­a
dc.contributor.editorUniversidad de Murcia, Departamento de Biologia Celular e Histiologia
dc.date.accessioned2026-05-07T08:50:43Z
dc.date.available2026-05-07T08:50:43Z
dc.date.issued2026
dc.description.abstractBackground. This study aimed to identify key molecules that potentially mediate the mechanisms by which YAP deletion or inhibition attenuates liver fibrosis. Materials and Methods. C57BL/6 mice were divided into four groups: control, carbon tetrachloride (CCl4), CCl4-YAP-HKO, and CCl4-verteporfin (VP). RNA sequencing (RNA-seq) and proteomic analysis were conducted. Immunohistochemistry and western blotting were also performed to verify the differentially expressed genes (DEGs) identified through the multi omics approach. Human subjects were enrolled to further assess the identified DEGs. Results. In comparison with the CCl4 group, both the CCl4-YAP-HKO and CCl4-VP groups exhibited liver fibrosis regression. RNA-seq and proteomic analyses identified 12 commonly differentially expressed molecules. Immunohistochemistry and western blotting validated that heat shock protein 27 (HSP27), heat shock protein 70 (HSP70), and p62 expression were significantly reduced, and milk fat globule-epidermal growth factor 8 (MFGE8) expression was elevated in both the CCl4-YAP-HKO and CCl4-VP groups compared with the CCl4 group. Furthermore, plasma p62, HSP27, and HSP70 levels were increased with the occurrence of chronic hepatitis B and HBV-related cirrhosis, whereas MFGE8 levels were decreased. Spearman’s correlation analysis further illustrated a significant association between these biomarkers and YAP levels. Conclusions. This study identified HSP27, HSP70, p62, and MFGE8 as crucial YAP-related molecules involved in liver fibrosis.
dc.formatapplication/pdf
dc.format.extent18
dc.identifier.doihttps://doi.org/10.14670/HH-18-993
dc.identifier.eissn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/230321
dc.languageeng
dc.relationSin financiaciĂłn externa a la Universidad
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectYes-associated protein
dc.subjectRNA sequencing
dc.subjectroteome sequencing
dc.subjectVerteporfin
dc.subjectLiver fibrosis
dc.subject.odsNo relacionado con ningĂşn objetivo de desarrollo sostenible
dc.titleUnraveling key molecules mediating the mechanisms of YAP deletion or inhibition in liver fibrosis regression through a multi-omics approach
dc.typeinfo:eu-repo/semantics/article
dspace.entity.typePublication
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Histology and histopathology, Vol.41, NÂş5, (2026)