Lipids & metabolic liver disease
Associations between cuprotosis‐related genes and the spectrum of metabolic dysfunction‐associated fatty liver disease: An exploratory study
Authors' conclusion
GLS may contribute to liver inflammation and fibrosis in MAFLD mainly through cuprotosis and T-cell activation, promoting the progression of MAFLD to HCC. These findings suggest that cuprotosis may play a role in MAFLD progression, potentially providing new insights into MAFLD pathogenesis.
Study context
- Population
- Patients across the MAFLD spectrum, including MAFLD-related hepatocellular carcinoma (HCC)
- Participants
- 331 / 271 / 656
- Comparison
- MAFLD vs MAFLD-related HCC vs Wenzhou PERSONS
- MAFLDn = 331
- MAFLD-related HCCn = 271
- Wenzhou PERSONSn = 656
- Outcome
- Associations of cuprotosis-related genes (CRGs) with the MAFLD spectrum
Methodological detailsbulk RNA sequencing datasets, single-cell RNA sequencing datasets, independent validation cohort
- Bulk RNA sequencing datasets
- Single-cell RNA sequencing datasets
- Independent validation cohort
Performance
As reported in the abstract
- GLS, GCSH and ATP7B differed significantly across the MAFLD spectrum and were significantly associated with liver fibrosis stages
- GLS closely associated with fibrosis stages in MAFLD and MAFLD-related HCC
- GLS predominantly expressed in monocytes and T cells in MAFLD
- GLS expression in T cells decreased during progression from metabolic dysfunction-associated fatty liver to metabolic-associated steatohepatitis
- GWAS: multiple SNPs in GLS associated with clinical indicators of MAFLD
Original publication
Associations between cuprotosis‐related genes and the spectrum of metabolic dysfunction‐associated fatty liver disease: An exploratory study. Diabetes Obes Metab. Published 16 September 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →