Breathing Easier

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Science  21 Jun 2002:
Vol. 296, Issue 5576, pp. 2103
DOI: 10.1126/science.296.5576.2103c

Respiratory distress syndrome (RDS) is one of the most common medical complications in infants delivered prematurely. This condition is often fatal and is caused by insufficient alveolar production of surfactant, a mixture of phospholipids and proteins that is essential for normal lung mechanics. The pathogenesis of RDS is not well understood.

A study of mouse models by Compernolle et al. reveals that vascular endothelial growth factor (VEGF), a secreted protein known for its role in promoting blood vessel growth, may also contribute to fetal lung maturation and thereby protect against RDS. Mice genetically deficient in certain isoforms of VEGF or in hypoxia-inducible factor 2α (HIF-2α), a transcription factor that regulates VEGF expression, were found to succumb to RDS soon after birth. VEGF stimulated surfactant production in cultured alveolar cells and improved lung function in mice with RDS when administered either in utero or immediately after birth. These results suggest that VEGF, which is already in clinical trials for therapeutic angiogenesis, may merit investigation as a possible treatment for RDS in premature babies. — PAK

Nature Med. 8, 10.1038/nm721 (2002).

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