Prevention and treatment of bronchopulmonary dysplasia: contemporary status and future outlook.
Despite tremendous advances in neonatology, bronchopulmonary dysplasia (BPD) remains a major cause of morbidity and mortality among premature infants. Any intervention that would reduce the risk of BPD or improve its outcome is likely to have substantial clinical and financial benefits. However, there is a clear lack of an effective agent for the treatment and/or prevention of BPD. This is due to an incomplete understanding of the molecular mechanisms involved in its pathogenesis. Taking a basic biological approach, our laboratory has discovered that disruption of normal alveolar homeostatic signaling is centrally involved in this process. Using a number of in vitro and in vivo models, our laboratory has demonstrated that stabilization of the normal alveolar homeostatic signaling pathway(s) can prevent and/or rescue the molecular injuries caused by the insults that lead to BPD. Here, we review the existing approaches to prevent and treat BPD and then, based on our insights into the pathogenesis of BPD, we propose novel and innovative therapeutic options that impact the disease on a cell/molecular level, unlike most of the current treatments available for BPD.
Cerny
Laura
L
Harbor-UCLA-CHOC Neonatal Perinatal Fellowship Program, Los Angeles Biomedical Research Institute at Harbor UCLA Medical Center, Torrance, California 90502, USA.
Torday
John S
JS
Rehan
Virender K
VK
D001997:Bronchopulmonary Dysplasia / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007235:Infant, Premature, Diseases / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control; D047495:PPAR gamma / Q000819:agonists; D044162:Parathyroid Hormone-Related Protein / Q000819:agonists; D015398:Signal Transduction / Q000502:physiology
D047495:PPAR gamma; D044162:Parathyroid Hormone-Related Protein