VIM and pulmonary fibrosis: Using mice lacking vimentin, a type III intermediate filament, Dos Santos and colleagues demonstrated an important role for vimentin in regulating NLRP3 inflammasome signaling that promotes acute lung injury, IL-1β expression, alveolar epithelial barrier permeability, and lung fibrosis following exposure to lipopolysaccharide (LPS), crocidolite asbestos, and bleomycin [119].