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Fibrosis
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Fibrosis is characterised by the excessive accumulation of extracellular matrix (ECM) due to a dysregulated wound healing response. Unchecked, severe fibrosis causes disruptions in tissue architecture, organ dysfunction, and ultimately organ failure. Fibrosis is also a common feature of many cancers, with up to 20% of cancers linked to fibrosis related to chronic inflammation. Despite a comprehensive understanding of the underlying pathobiology of fibrosis there remains a translational gap between the identification of antifibrotic targets and the transition to effective patient therapies
Fibrosis is a complex process involving multiple different cell types interacting within the diseased tissue environment. Central to this is the scar-producing myofibroblast which are responsible for ECM production. These cells are widely considered to arise predominantly from the activation of resident mesenchymal cells (i.e, fibroblasts and pericytes). Understanding the molecular mechanisms that underpin this process has become a key focus in the development of novel antifibrotic therapies.
To address this, we aim to provide comprehensive solutions to aid antifibrotic drug development and clinical trial output analysis.
Cell Based Assays: Assess mesenchymal cell function in monoculture and co-culture assays. Readouts include, but are not limited to cell activation, collagen production, migration, and proliferation.
3D Spheroid Fibrosis Models: Test your antifibrotic therapies through development of bespoke epithelial and mesenchymal 3D models with immune cell co-culture.
Spatial Biology: Use our comprehensive suite of GCP compliant Histology services and integrated image analysis to aid target validation, biomarker assay development, and further your understanding of anti-fibrotic drug response and mechanism of action.
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