PMC:7319613 / 6237-7420 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":"In summary, prematurely born COVID-19 patients could be particularly vulnerable to both infection and adverse outcome. High ACE2 activity levels may enable enhanced virus-binding, thus increasing infection risk. A pre-existing adverse redox balance could then contribute to the aggravation of inflammatory mechanisms by oxidation of different biomolecules including phospholipids, incidentally exacerbating vascular and lung injury. Oxidative damage to oxygen-sensing mitochondria in conjunction with COVID-19-related hypoxemia and prematurity-associated ventilator response deficits may synergistically deteriorate the health status facilitated by a potentially compromised respiratory system of the prematurely born individual. We believe that the above-summarized data and mechanisms observed in prematurely born individuals should be considered when managing/treating COVID-19 patients. As no sound epidemiological data currently exist on the topic, future epidemiological and experimental efforts are urgently warranted to elucidate the relationship between prematurity and COVID-19 severity and thereby optimize therapeutic approaches for this, up-to-now neglected, 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