Study of overall survival associated with nintedanib and pirfenidone in patients with idiopathic pulmonary fibrosis: a real-life comparison

Mazzoleni, Ludovica; Borsino, Cecilia; Zovi, Andrea

doi:10.1136/ejhpharm-2021-003202

Cited by 3 publications

(2 citation statements)

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“…Lung fibrosis, including idiopathic pulmonary fibrosis, is treated with nintedanib and pirfenidone 7 . Although these drugs have significantly enhanced the condition of patients with lung fibrosis in clinical trials 8 , 9 , prognosis remains to be improved 10 . Long-term observation of 263 patients with idiopathic pulmonary fibrosis has shown that their median survival is 1224 days 11 .…”

Section: Introductionmentioning

confidence: 99%

“…Several clinical studies have indicated that immune checkpoint inhibitors, including anti-programmed cell death-1 inhibitors, sometimes cause interstitial pneumonia; once interstitial pneumonia occurs, therapeutic options become limited 6 .Lung fibrosis, including idiopathic pulmonary fibrosis, is treated with nintedanib and pirfenidone 7 . Although these drugs have significantly enhanced the condition of patients with lung fibrosis in clinical trials 8,9 , prognosis remains to be improved 10 . Long-term observation of 263 patients with idiopathic pulmonary fibrosis has shown that their median survival is 1224 days 11 .…”

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confidence: 99%

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Plant miRNA osa-miR172d-5p suppressed lung fibrosis by targeting Tab1

Kumazoe

Ogawa

Hikida

et al. 2023

Sci Rep

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Lung fibrosis, including idiopathic pulmonary fibrosis, is an intractable disease accompanied by an irreversible dysfunction in the respiratory system. Its pathogenesis involves the transforming growth factorβ (TGFβ)-induced overproduction of the extracellular matrix from fibroblasts; however, limited countermeasures have been established. In this study, we identified osa-miR172d-5p, a plant-derived microRNA (miR), as a potent anti-fibrotic miR. In silico analysis followed by an in vitro assay based on human lung fibroblasts demonstrated that osa-miR172d-5p suppressed the gene expression of TGF-β activated kinase 1 (MAP3K7) binding protein 1 (Tab1). It also suppressed the TGFβ-induced fibrotic gene expression in human lung fibroblasts. To assess the anti-fibrotic effect of osa-miR172d-5p, we established bleomycin-induced lung fibrosis models to demonstrate that osa-miR172d-5p ameliorated lung fibrosis. Moreover, it suppressed Tab1 expression in the lung tissues of bleomycin-treated mice. In conclusion, osa-miR172d-5p could be a potent candidate for the treatment of lung fibrosis, including idiopathic pulmonary fibrosis.

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