Scientific and clinical studies have demonstrated that insufficient or impaired mitophagy – a process where dysfunctional mitochondria are selectively cleared from the cell – is involved in IPF pathogenesis (Kurita et al Respiratory Research, 2017 18:114). Insufficient mitophagy in IPF has been implicated in both increasing apoptosis and cellular senescence in epithelial lung cells and enhancing fibrogenic myofibroblast differentiation in lung fibroblasts.
There is a significant unmet medical need for the treatment of IPF, as current therapies are limited to reducing certain symptoms only.
Therefore activating mitophagy through USP30 inhibition has the potential to be a promising therapeutic approach for treating IPF.
- Dr Nick Edmunds Appointed to VP, Head of DUB Discovery3rd December 2018
- Mission Therapeutics and AbbVie sign DUBs Collaboration in Alzheimer’s and Parkinson’s Disease15th November 2018
- Mission Therapeutics Strengthens Clinical Development Team with Appointment of Dr Judit Molnar as Senior Director, Translational Medicine4th September 2018