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The toxicity of silica nanoparticles (SiNPs) to lung is known. We previously demonstrated that exposure to SiNPs promoted pulmonary impairments, but the precise pathogenesis remains elucidated. Ferroptosis has now been identified as a unique form of oxidative cell death, but whether it participated in SiNPs-induced lung injury remains unclear. In this work, we established a rat model with sub-chronic inhalation exposure of SiNPs via intratracheal instillation, and conducted histopathological examination, iron detection, and ferroptosis-related lipid peroxidation and protein assays. Moreover, we evaluated the effect of SiNPs on epithelial ferroptosis, possible mechanisms using in vitro -cultured human bronchial epithelial cells (16HBE), and also assessed the ensuing impact on fibroblast activation for fibrogenesis. Consequently, fibrotic lesions occurred in the rat lungs, concomitantly by enhanced lipid peroxidation, iron overload, and ferroptosis. Consistently, the in vitro data showed SiNPs triggered oxidative stress and caused the accumulation of lipid peroxides, resulting in ferroptosis. Importantly, the mechanistic investigation revealed miR-21-5p as a key player in the epithelial ferroptotic process induced by SiNPs via targeting GCLM for GSH depletion. Of note, ferrostatin-1 could greatly suppress ferroptosis and alleviate epithelial injury and ensuing fibroblast activation by SiNPs. In conclusion, our findings first revealed SiNPs triggered epithelial ferroptosis through miR-21-5p/GCLM signaling and thereby promoted fibroblast activation for fibrotic lesions, and highlighted the therapeutic potential of inhibiting ferroptosis against lung impairments upon SiNPs exposure. [Display omitted] • Ferroptosis is discovered to be a new form of cell death upon SiNPs exposure. • miR-21-5p was a key player in epithelial ferroptosis by SiNPs via targeting GCLM. • SiNPs-elicited epithelial ferroptosis promoted fibroblast activation. • Anti-ferroptosis strategies maybe a promising strategy for fibrotic lung diseases. [ABSTRACT FROM AUTHOR]

Based on the wear analysis of a propeller hub bearing, wear tests are designed under different marine environments to illustrate wear failure mechanisms. The results reveal that the wear failure characteristics of the propeller hub bearing are primarily abrasive wear, accompanied by adhesion and oxidation wears, and plastic deformation. These results agree well with the wear morphologies of the torsional fretting wear tests under starvation lubrication. The wear tests confirm that the wear failure of the propeller hub bearing is owing to the coexistence of multiple wear mechanisms, which is attributed primarily to the superimposed wear behaviors induced by loading, continuous fretting wear, and starvation lubrication in the local contact areas. Hence, the negative effects of interfacial micro-protrusion adhesion and fracture during oil lubrication are difficult to eliminate. Moreover, The uneven radial loads of the contact surfaces of the propeller hub bearing also exhibit a significant influence on the thickness and formation of the oil film at the friction interface. [Display omitted] • Wear failure mechanisms of bearing coated with NAB alloys had been studied. • The designed wear tests were conducted by a self-assemble tribological platform. • Wear failure morphologies of bearing and wear tests results had been discussed. • Physical model at the different wear stages was established. [ABSTRACT FROM AUTHOR]