SIRT3 and pulmonary fibrosis: Taken together, these findings suggest that SIRT3 is crucial for maintaining mtDNA integrity in the setting of fibrogenic oxidative stress and thereby limits AEC apoptosis and lung fibrosis; however, it is unclear whether transgenic whole body SIRT3 overexpression (Sirt3Tg) mice are protected against lung fibrosis following asbestos exposure, a non-resolving model of lung fibrosis unlike bleomycin, and if so, whether the protective effects are mediated in part by attenuating lung and AEC mtDNA damage and recruitment of Mo-AMs.