1. Academic Validation
  2. Cyp7a1 and Cyp8b1 Downregulation Characterizes Concanavalin-A-Induced Acute Liver Injury: Insights from Multiomics Analysis

Cyp7a1 and Cyp8b1 Downregulation Characterizes Concanavalin-A-Induced Acute Liver Injury: Insights from Multiomics Analysis

  • J Proteome Res. 2025 Dec 31. doi: 10.1021/acs.jproteome.5c00646.
Xinlei Liu 1 2 Rui Liu 3 Meng Zhang 3 Di Ma 3 Yingming Tian 3 Yancheng Wang 4
Affiliations

Affiliations

  • 1 Laboratory Animal Research Center, School of Medicine, Chongqing University, Chongqing 400044, China.
  • 2 Key Laboratory of Biorheological Science and Technology Ministry of Education College of Bioengineering, Chongqing University, Chongqing 400044, China.
  • 3 Institute for Immunology and Pathogenesis, Chongqing Medical University, Chongqing 400016, China.
  • 4 State Key Laboratory of Power Transmission Equipment Technology, School of Electrical Engineering, Chongqing University, Chongqing 400044, China.
Abstract

Concanavalin-A (ConA)-induced acute liver injury (ALI) is a widely used model for immune-mediated liver damage, but its molecular mechanisms remain poorly understood. We applied a multiomics approach that integrates transcriptomics, metabolomics, and proteomics to characterize the pathogenic features of ConA-induced ALI. Our analysis revealed significant downregulation of Cyp7a1 and Cyp8b1, two key Enzymes in bile acid biosynthesis, as potential hallmark features of this model. Mechanically, suppression of these genes was correlated with altered bile acid metabolism, increased proinflammatory cytokine production (e.g., TNF-α, IL-6, and IL-1β), and elevated markers of hepatocyte Apoptosis. Furthermore, multiomics network analysis highlighted interactions among bile acid dysregulation, oxidative stress, and immune activation, suggesting a synergistic role in ConA-induced liver injury. These findings improve our understanding of immune-mediated ALI and suggest the downregulation of Cyp7a1/Cyp8b1 as a diagnostic marker or therapeutic target for acute hepatotoxicity.

Keywords

acute liver injury; biomarker; concanavalin A; inflammation; liver damage; multiomics.

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