{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T21:51:14Z","timestamp":1787349074886,"version":"build-2736575974"},"reference-count":22,"publisher":"Georg Thieme Verlag KG","issue":"S 01","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Am J Perinatol"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:p>Bronchopulmonary dysplasia (BPD) and poor neurodevelopmental outcome after preterm birth are closely associated. However, mechanistic links are uncertain. We are exploring the hypothesis that decreased circulating insulin-like growth factor (IGF)-1 after preterm birth due to the abrupt end of supply by the placenta impairs growth during critical windows of development in most organs, including the lung and brain. Throughout gestation, the fetus uses glycolysis as its main source of energy. Metabolism is mainly stopped at pyruvate, which serves as a \u201cmetabolic crossroad\u201d, allowing for the production of amino acids and other \u201cbuilding blocks\u201d for new cells. Metabolic pathways are differentially regulated in the nucleus and the cytoplasm. The ratio between pyruvate dehydrogenase (PDH) and pyruvate dehydrogenase kinase (PDK) determines the biochemical activity which irreversibly metabolizes pyruvate to acetyl-co-A. Metabolites in the nucleus modulate epigenetic remodeling, an essential mechanism of normal growth and maturation during development. IGF-1 has been shown to contribute significantly to the development of virtually all organs, especially related to the regulation of microvascular growth, based on extensive studies of the brain, retina, lung, and intestine. With a preterm birth, the abrupt withdrawal of the placental supply of IGF-1 and its local production directly affects metabolism and microvascular development, which may contribute to a high risk for organ maldevelopment and injury after birth. We speculate that reduced bioavailability of IGF-1 is a possible link between lung and brain development disruption and increases susceptibility for major pulmonary and neurocognitive morbidities in preterm babies.<\/jats:p><jats:p>\n            Key Points\n          <\/jats:p>","DOI":"10.1055\/s-0042-1756677","type":"journal-article","created":{"date-parts":[[2022,11,1]],"date-time":"2022-11-01T23:55:57Z","timestamp":1667346957000},"page":"S14-S17","source":"Crossref","is-referenced-by-count":18,"special_numbering":"S","title":["Bronchopulmonary Dysplasia and Impaired Neurodevelopment\u2014What May Be the Missing Link?"],"prefix":"10.1055","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7682-2591","authenticated-orcid":false,"given":"Boris W.","family":"Kramer","sequence":"additional","affiliation":[{"name":"University of Western Australia, Subiaco, Western Australia, Australia"},{"name":"Neuroplast BV, Maastricht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victoria","family":"Niklas","sequence":"additional","affiliation":[{"name":"Oak Hill Bio Ltd., 1 Ashley Road, Altrincham, Cheshire, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven","family":"Abman","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Division of Pulmonology, University of Colorado Anschutz Medical Center, Aurora, Colorado"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"194","published-online":{"date-parts":[[2022,11,1]]},"reference":[{"issue":"03","key":"ref1","doi-asserted-by":"crossref","first-page":"239","DOI":"10.3233\/NPM-190303","article-title":"Microglia: newly discovered complexity could lead to targeted therapy for neonatal white matter injury and dysmaturation","volume":"12","author":"J J Volpe","year":"2019","journal-title":"J Neonatal Perinatal 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