CORD-19:0376103fd7863b10e41a0f59fe226be9765f34c7 / 0-1440 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/CORD-19/sourceid/0376103fd7863b10e41a0f59fe226be9765f34c7","sourcedb":"CORD-19","sourceid":"0376103fd7863b10e41a0f59fe226be9765f34c7","text":"Cell-Based Strategies to Reconstitute Lung Function in Infants with Severe Bronchopulmonary Dysplasia\n\nAbstract\n\n\nExtreme prematurity is one of the major risk factors for the development of chronic lung disease of prematurity or bronchopulmonary dysplasia (BPD). 1 Preterm infants born between 24 and 28 weeks of gestation (ie, extremely preterm) have an immature pulmonary surfactant system, immature airway and vascular architecture, and an underdeveloped surface area for gas exchange (Fig. 1) . 2 Many very preterm infants require prolonged respiratory support to ensure survival, which further increases their risk of developing BPD.\nRecent evidence suggests that BPD may have long-term respiratory complications that reach beyond childhood. Numerous follow-up studies indicate that children and young adults who were born very preterm are at an increased risk of respiratory symptoms, poor lung function, and lower exercise capacity [3] [4] [5] [6] [7] this is especially apparent in infants who have developed BPD. More alarmingly, isolated case studies are surfacing of irreversible arrested alveolar development at adult age in former premature infants with BPD, 8, 9 mirroring results from experimental models of BPD. 10 Progress toward decreasing the incidence/severity of BPD over the next few years using currently available techniques and strategies is likely (ie, optimization of antenatal management combined with 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