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Slowing fibrosis

Professor Tim Johnson (University of Sheffield, and UCB New Medicines) discussed the implication of fibrosis (see table 1) in organ scarring in the Western world, indicating that it is involved in 45% of all organ death. Our targeting for future therapeutics, however, hasn’t been particularly successful of yet.

One example is tissue growth factor (TGF-β), which is a powerful regulator of fibrotic disease throughout the body. Despite the money spent by drug companies to investigate this, the autoimmune side effects have been too widespread. Similarly, peroxisome proliferator-activated receptor (PPAR) agonists are used in diabetes and hyperlipidaemia, but their adverse effects profiles – particularly fluid retention and decompensation of heart failure symptoms – have prevented use as an antifibrotic drug in patients.

Table 1. The six key pillars of fibrosis

Table 1. The six key pillars of fibrosis

More promisingly, lysophosphatidic acid receptors (LPAR) are associated with cell proliferation and maintenance throughout the body. This is thought to be associated with increased intracellular calcium mobilisation. The signalling pathway associated with this is thought to directly contribute to several diseases and, as such, several receptor antagonists are currently in phase II production. They have shown promising results with regards to fibrosis and, along with autotaxin inhibition, may become available for use in the coming years.1 It is likely, though, that we will need to consider multi-drug therapies if we are to slow organ death associated with fibrosis.

References

1. Stoddard NC, Chun J. Promising pharmacological directions in the world of lysophosphatidic acid signaling. Biomol Ther 2015;23:1–11. http://dx.doi.org/10.4062/biomolther.2014.109

Published on: February 21, 2017

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