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Palabras clave – provistas por la editorial

interstitial fibrosis; lung; alveolar fibroelastosis; idiopathic pulmonary fibrosis; pirfenidone; nintedanib; discontinuation; body mass index; adverse event; antifibrotic treatment; IPF; alveolar epithelial cells; intermediate epithelial cells; transitional states; LysoTracker; flow cytometry; lung transcriptomic profile; CK5; NGFR; CD24; epidermal growth factor; epidermal growth factor receptor; ErbB-signaling; pulmonary fibrosis; lung fibrosis; tyrosine kinase inhibitor; TGF-α; TGF-β; amphiregulin; neuregulin 1; basal cells; bronchial epithelium; airway epithelium; MUC5B; single cell RNA sequencing; epithelial populations; antibody folding; immunophilin; interstitial lung disease; ER stress; tacrolimus; FK506-binding protein; peptidyl-prolyl isomerase; 3D cultures; IPF modelling; drug screening; idiopathic pulmonary fibrosis (IPF); histone deacetylase (HDAC); histone acetylation; non-histone protein acetylation; fibroblast-to-myofibroblast differentiation (FMD); type-II alveolar epithelial cell (AECII); bronchiolar basal cells; bronchiolization; Class I-HDAC-inhibitor; (pan-)HDAC-inhibitor; IGF1; IGF1R; lung development; bleomycin-induced pulmonary fibrosis; bleomycin; recombinant FGF10; alveolar epithelial progenitors; AT2 cells; n/a