Mitochondria-target ubiquinone attenuates bleomycin-induced pulmonary fibrosis.

Background: Pulmonary fibrosis arises from various etiologies, often associated with elevated levels of reactive oxygen species (ROS) stress and activation of pro-fibrotic signaling pathways. The chemotherapeutic drug bleomycin has been shown to exacerbate pulmonary fibrosis during anti-tumor treatment. Further research is needed to combat bleomycin-induced fibrosis. Aim: This investigation aims to identify critical mediators of bleomycin-induced pulmonary fibrosis and evaluate the therapeutic potential of mitochondria-targeted ubiquinone (MitoQ) in attenuating fibrotic pathogenesis. Methods: A bleomycin-induced pulmonary injury mouse model and fibroblast cell culture were established, followed by histopathology evaluation, molecule interaction analysis, cytokine quantification, intervention assay, and flow cytometry. Results: We analyzed RNA-seq data from a bleomycin-induced pulmonary fibrosis mouse model and identified a network of oxidative stress-related fibrosis genes centered on Tgfb1. In fibroblast cell lines, bleomycin exposure elevated mitochondrial and cellular ROS, increased mitochondrial mass and the MDR Conclusion: These findings not only advance our understanding of the interplay between oxidative stress and pro-fibrotic signaling in bleomycin-induced pulmonary fibrosis but also provide experimental data supporting the use of mitochondria-targeted antioxidant in the treatment of this condition.