【摘 要】
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Dear Editor,rnMitochondrial complex Ⅰ is important for cellular ATP pro-duction by transporting electrons and generating proton gradient across the mitochondri
【机 构】
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Cardiovascular Research Institute and Department of Physiology, University of California San Francis
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Dear Editor,rnMitochondrial complex Ⅰ is important for cellular ATP pro-duction by transporting electrons and generating proton gradient across the mitochondrial inner membrane (Hirst, 2013). It is also a major cellular locus where electron leakage to oxygen produces superoxide, an ROS (reactive oxygen species), particularly under oxidative stress conditions. Dysfunctional complex Ⅰ contributes to the most common oxidative phosphorylation disorder in humans, with many identified genetic mutations in complex Ⅰ subunits causing a variety of human disorders including Leigh syndrome, encephalomyopathy, cardiomyopathy, parkinsonism and hereditary optic neuropathy (Hirst, 2013;Guo et al., 2017). In addition, complex Ⅰ is the major target of many parkinsonism-causing neurotoxins including rotenone and MPTP. Past biochemical, cell biological and structural studies have elu-cidated how complex Ⅰ functions normally in mitochondrial respiration (Hirst, 2013;Guo et al., 2017;Letts and Sazanov, 2017). Nonetheless, our understanding of mechanisms how complex Ⅰ dysfunction leads to human diseases is far from completion; therapeutic targets and strategies are urgently needed.
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