In Vitro Liver Fibrosis 2D/3D Research Models



Model Overview


In vitro liver fibrosis models simulate the pathological accumulation of extracellular matrix (ECM) proteins (e.g., collagen, fibronectin) in response to chronic liver injury. These models are essential for studying fibrogenesis mechanisms, anti-fibrotic drug screening, and therapeutic validation.


1. 2D Liver Fibrosis Models

  • Construction:

    • Hepatic stellate cells (HSCs) are activated in monolayer culture using pro-fibrotic stimuli (e.g., TGF-β1, PDGF).

    • Co-culture with hepatocytes, Kupffer cells, or endothelial cells to mimic cell-cell crosstalk.

  • Applications:

    • High-throughput screening of anti-fibrotic agents.

    • Mechanistic studies of HSC activation (e.g., α-SMA expression, ECM secretion).

  • Advantages:

    • Cost-effective, scalable, and compatible with molecular biology assays (e.g., qPCR, Western blot).


2. 3D Liver Fibrosis Models

  • Construction:

    • 3D spheroids/organoids: Co-culture HSCs, hepatocytes, and NPCs in ECM-rich matrices (e.g., collagen, Matrigel).

    • Bioengineered scaffolds: Decellularized liver scaffolds or synthetic hydrogels to mimic fibrotic tissue stiffness.

    • Microfluidic systems: Simulate dynamic nutrient/cytokine gradients and shear stress.

  • Applications:

    • Study ECM remodeling and mechanotransduction in fibrosis.

    • Evaluate drug penetration and efficacy in a pathophysiologically relevant microenvironment.

  • Advantages:

    • Recapitulate spatial ECM depositionhypoxic zones, and immune cell infiltration seen in vivo.

    • Support long-term modeling of fibrosis progression and regression.


Key Features

  • Pathological Biomarkers:

    • Quantify collagen deposition (Sirius Red staining, hydroxyproline assays).

    • Assess α-SMA (activated HSC marker), TIMP-1, and MMP activity.

  • Functional Assays:

    • Stiffness measurement via atomic force microscopy (AFM).

    • Hypoxia imaging (pimonidazole staining).


Technical Capabilities

  • Customizable Models:

    • Disease-specific fibrosis (e.g., NASH-driven, viral hepatitis-driven).

    • Species-specific (human, mouse, rat) or patient-derived cells.

  • Multi-Omics Integration:

    • Transcriptomics, proteomics, and metabolomics to map fibrotic pathways.


Why Choose Our Models?

Developed by a team with 14+ years of liver research expertise, our fibrosis models bridge the gap between simplistic in vitro systems and complex in vivo biology, accelerating drug discovery and mechanistic breakthroughs.