Oxidative stress appears to play a role in the pathogenesis of IPF (Kinnula,V.L. et al., 2008; Janssen-Heininger,Y.M. et al., 2010; Kurundkar,A. & Thannickal,V.J., 2016).
In 2018 Anathy et al. have shown a potential new treatment for IPF by the reduction of protein oxidation in the lung. This research group showed that fibrotic lungs have decreased GLRX (glutaredoxin-1) enzymatic activity and increased PSSG (protein S-glutathionylation) activity. Protein S-glutathionylation (PSSG) is a post-translational modification of proteins which contributes to the apoptotic pathway. PSSG can be reversed by glutaredoxin-1 (GLRX). Direct administration of Glrx protein into airways reversed increases in collagen in mice with TGFβ1- or bleomycin-induced fibrosis thus showing that GLRX and PSSG play a role in lung fibrosis. Exogenous GLRX may potentially be used to treat lung fibrosis and so give hope to the many sufferers of IPF.
Anathy,V., Lahue,K.G. et al., (2018) Reducing protein oxidation reverses lung fibrosis. Nature Medicine 24, 1128 – 1135.
Janssen-Heininger, Y. M. et al. Regulation of apoptosis through cysteine oxidation: implications for fibrotic lung disease. Ann. NY Acad. Sci. 1203, 23–28 (2010).
Kinnula, V. L. & Myllarniemi, M. Oxidant–antioxidant imbalance as a potential contributor to the progression of human pulmonary fibrosis. Antioxid. Redox Signal. 10, 727–738 (2008).
Kurundkar, A. & Thannickal, V. J. Redox mechanisms in age-related lung fibrosis. Redox Biol. 9, 67–76 (2016).