Increased procoagulant and antifibrinolytic activities in the lungs with idiopathic pulmonary fibrosis
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2023, Respiratory Medicine and ResearchTargeting PI3K/AKT signaling for treatment of idiopathic pulmonary fibrosis
2022, Acta Pharmaceutica Sinica BCommon Co-Morbidities in Fibrosing Interstitial Lung Disease
2021, Encyclopedia of Respiratory Medicine, Second EditionModeling of Fibrotic Lung Disease Using 3D Organoids Derived from Human Pluripotent Stem Cells
2019, Cell ReportsCitation Excerpt :To examine to what extent the findings in our HPS mutant organoid model would also be applicable to IPF, we re-analyzed publicly available datasets of human IPF patient samples, with the caveat that while our studies were performed on purified epithelial cells, genome-wide expression profiling in IPF is performed on tissue samples containing both epithelium and abundant mesenchymal cells. The shared upregulated genes in HPS1−/− and HPS2−/− organoids included SERPINE1 (also known as PAI-1), a well-known biomarker of IPF (Kotani et al., 1995) and of fibrosis in mice treated with bleomycin (Fernandez et al., 2016), and FN, an ECM component. We confirmed increased FN (Figures 2B and 2D) and PAI-1 (Figure S4B) expression in HPS1−/− and HPS2−/− organoids, whereas no increased expression was observed in HPS8−/− organoids.
The impaired proteases and anti-proteases balance in Idiopathic Pulmonary Fibrosis
2018, Matrix BiologyCitation Excerpt :However, in fibrotic lungs, the extravascular fibrin is not effectively cleared, and epithelial repair is blocked due to a marked increase of serpins, in particular PAI-1, relative to uPA [158,159]. Indeed, high levels of the serpin PAI-1 have been observed in IPF and are associated with poor clinical outcomes [160,161]. Moreover, Pai1-deficient mice are relatively protected from developing pulmonary fibrosis induced by bleomycin, and the beneficial effect of Pai1 deficiency was associated with proteolytic activity of the plasminogen activation system [162,163].
The fibrogenic actions of the coagulant and plasminogen activation systems in pulmonary fibrosis
2018, International Journal of Biochemistry and Cell BiologyCitation Excerpt :In interstitial tissue, uPA drives plasminogen activation, initiating non-fibrinolytic actions of plasmin such as pericellular proteolysis and cell activation (Del Rosso et al., 2011). The accumulation of airspace fibrin in IPF is in large part a consequence of suppressed fibrinolysis due to local increases in the serpins, plasminogen activator inhibitor-1 (PAI-1) and α2-antiplasmin (Kotani et al., 1995; Gunther et al., 2000; Chambers and Scotton, 2012). However, increased levels of fibrin D-dimer, a FDP detected in the serum and BALF of IPF patients is evidence that fibrinolysis occurs, albeit not at a rate sufficient to counter net fibrin formation (Nakstad et al., 1990; Bargagli et al., 2014).