Mitochondrial TOM70 in Hyperoxia-induced Acute Lung Injury.

TLR4 deficiency decreased TOM70 expression and induced mitophagy and mitochondrial fusion, indicating that TOM70 is regulated by TLR4. Silencing TOM70 resulted in increased mitochondrial fusion and fission in MLEC, suggesting that TOM70 impacts mitochondrial quality control in mammalian, primary cells (MLEC) that are critical for lung airspace barrier function. Hyperoxia decreased TOM70 protein expression in mouse lungs, which may be a potential mechanism whereby hyperoxia leads to respiratory failure. Given that TOM70 maintains mitochondrial health, our data suggest that TOM70 may play a key role in the pathological mechanisms of HALI. 1. Liu et al. (2021) bioRxiv, 2. Zhang et al. (2019) Antioxid Redox Signal, 3. Zhang et al. (2016) Antioxid Redox Signal, 4. Takyar et al. (2015) FASEB J. 5. Kim et al. (2019) Aging Cell. 6. Zhang et al. (2021) AJP Lung Cell Mol Physiol.