Journal
BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
Volume 100, Issue 3, Pages 158-167Publisher
WILEY
DOI: 10.1002/bdra.23237
Keywords
preterm; metalloproteinases; VEGF; genetics; airway; alveolarization; lung function
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Funding
- Programme Hospitalier de Recherche Clinique [PHRC AOR 07 018]
- Agence Nationale de la Recherche [ANR-09-GENO-037, ANR-BLANC-12-BSV1-0004-01]
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Bronchopulmonary dysplasia (BPD) is the main respiratory sequela of extreme prematurity. Its pathophysiology is complex, involving interactions between host and environment, likely to be significantly influenced by genetic factors. Thus, the clinical presentation and histological lesions have evolved over time, along with the reduction in neonatal injuries, and the care of more immature children. Impaired alveolar growth, however, is a lesion consistently observed in BPD, such that it is a key feature in BPD, and is even the dominant characteristic of the so-called new forms of BPD. This review describes the key molecular pathways that are believed to be involved in the genesis of BPD. Much of our understanding is based on animal models, but this is increasingly being enriched by genetic approaches, and long-term respiratory functional studies. Birth Defects Research (Part A) 100:158-167, 2014. (c) 2014 Wiley Periodicals, Inc.
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