Unraveling key molecules mediating the mechanisms of YAP deletion or inhibition in liver fibrosis regression through a multi-omics approach.
Abstract
BACKGROUND: This study aimed to identify key molecules that potentially mediate the mechanisms by which YAP deletion or inhibition attenuates liver fibrosis. MATERIALS AND METHODS: -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: 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.
Fields of Study & Subjects
Hippo pathway signaling and YAP/TAZ
Liver physiology and pathology
Connective Tissue Growth Factor Research
Publication details
- Journal / source
- PubMed
- Volume
- 41
- Issue
- 5
- Pages
- 831–848
- Publication date
- 1 May 2026
- Language
- EN