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c-Rel orchestrates energy-dependent epithelial and macrophage reprogramming in fibrosis

Here FibroFind scientists collaborated in a study led by Professor Fiona Oakley (FibroFind founding scientists and Director) that describes how a factor (c-Rel) that is best known for its role in the immune system also controls metabolic processes that are important for fibrosis. The identified c-Rel/Pfkfb3 pathway is proposed as a target for the development of anti-fibrotic drugs.

The FibroFind precision-cut liver slice model and its proprietary tissue bioreactor technology was vital to this work.

Neutrophils induce paracrine telomere dysfunction and senescence in ROS‐dependent manner

In this study which was co-led by FibroFind Chief Scientific Officer, Professor Derek Mann, the neutrophil which defends against infection can stimulate cellular senescence, this a condition in which cells adopt a pro-inflammatory state. As neutrophils accumulate in chronic diseases this discovery reveals a new mechanism by which inflammation is perpetuated and identifies the neutrophil as a target for therapeutic manipulation.

FibroFind’s proprietary tissue bioreactor technology was vital to this work in showing that neutrophils can cause hepatocytes within intact human liver to undergo senescence, this represents a major advance in being able to study senescence in an intact human tissue system.

A Bioreactor Technology for Modeling Fibrosis in Human and Rodent Precision-Cut Liver Slices

Fibrofind is able to keep human organ slices in an intact and active state for 7 days. We have optimised induction of fibrogenesis/fibrosis in normal PCS using a specific set of stimuli, which we are able to readily block using an inhibitor, this providing a positive control for any treatment that you may want us to test.

Our technology platform is detailed in our recently published paper in Hepatology journal that describes the PCLS (Liver) technology and associated outputs