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.
- Mission Therapeutics’ Highlights Positive Parkinson’s Disease USP30 Target and Inhibitor Data at the Society for Neuroscience 2017 Annual Meeting16th November 2017
- Mission Therapeutics’ Scientists Presenting Novel Parkinson’s USP30 Target and Inhibitor Data at the Society for Neuroscience 2017 Annual Meeting1st November 2017
- Mission Therapeutics Presenting at The Michael J. Fox Foundation’s Parkinson’s Disease Therapeutics Conference30th October 2017