PMC:7319613 / 4062-4649 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7319613","sourcedb":"PMC","sourceid":"7319613","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7319613","text":"It is well established that oxygen sensing in the lung and carotid bodies depends on mitochondrial function. The known vulnerability of mitochondria to oxidative stress suggests an additional feature of prematurity to be relevant for impaired oxygen sensing and COVID-19 severity; potentially higher oxidative stress levels as compared to full-term born individuals (Filippone et al., 2012; Martin et al., 2018). This difference in redox balance has indeed been hypothesized to be directly involved in the modulation of the ventilatory response to hypoxaemia in prematurely born 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