Long-term silica exposure to silica dust leads to irreversible pulmonary fibrosis, during which lung fibroblast activation plays an essential role. Mitochondria-associated endoplasmic reticulum membranes (MAMs) is a structural interface for communication between the outer mitochondrial membrane and the endoplasmic reticulum. VAPB-PTPIP51 is a key complex on MAMs. However, the role of VAPB-PTPIP51-linked MAMs in lung fibroblast activation remains under investigation. In this study, we observed mitochondrial damage and endoplasmic reticulum stress in a SiO-induced lung fibrosis model using C57BL/6J mice. In the model of TGF-β1-induced mouse lung fibroblast (MLG) activation, interventions with Dioscin and TUDCA reduced mitochondrial damage and alleviated endoplasmic reticulum stress by repairing damaged MAMs. Additionally, TUDCA may restore the MAMs structure by enhancing the interaction between VAPB and PTPIP51. Our findings indicate that MAMs may play a crucial role in linking mitochondrial damage and endoplasmic reticulum stress, suggesting their potential involvement in fibroblast activation.
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