Identification of CDKN1A as a potential key risk factor in MASLD progression
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View abstract on PubMed
Summary
This summary is machine-generated.Metabolic dysfunction-associated steatotic liver disease (MASLD) shows increased CDKN1A gene and protein levels, correlating with disease severity. This suggests CDKN1A may be a potential biomarker and therapeutic target for MASLD.
Area Of Science
- Hepatology
- Molecular Biology
- Genomics
Background
- Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly NAFLD, is a heterogeneous liver condition with unclear progression mechanisms.
- Lack of reliable diagnostic markers and effective treatments hinders MASLD management.
- Understanding MASLD pathogenesis is crucial for developing targeted therapies.
Purpose Of The Study
- To identify key genes involved in MASLD progression.
- To investigate the role of CDKN1A in MASLD pathogenesis.
- To evaluate CDKN1A as a potential diagnostic biomarker and therapeutic target for MASLD.
Main Methods
- Differential gene expression analysis of public MASLD datasets (GSE126848, GSE135251) using DESeq2 and edgeR.
- Protein-protein interaction network analysis to identify hub genes.
- Validation of CDKN1A expression in MASLD patient liver samples and animal models (HFD, ob/ob, db/db mice).
- Correlation analysis of CDKN1A levels with MASLD severity, NAS, and fibrosis stage.
Main Results
- 52 differentially expressed genes (DEGs) were identified in MASLD.
- Top 10 hub genes were identified through PPI network analysis.
- CDKN1A was the sole consistently upregulated gene in MASLD across multiple datasets and validated at protein level.
- CDKN1A mRNA and protein levels were significantly elevated in MASLD patients and animal models.
- CDKN1A expression correlated positively with MASLD severity, NAS, and fibrosis stage.
Conclusions
- CDKN1A is significantly upregulated in MASLD and its levels correlate with disease severity.
- CDKN1A shows potential as a promising biomarker for MASLD diagnosis and prognosis.
- CDKN1A may represent a novel therapeutic target for MASLD, warranting further investigation into its pathological role.
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