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Bronchopulmonary dysplasia is a common long-term consequence of prematurity. Using a rat model, Vaidya et al. found that the expression of CCN1, a cysteine-rich protein member of the CCN family of matricellular proteins, was downregulated by hyperoxia. Intraperitoneal administration of CCN1 reduced measures of pulmonary inflammation, vascular remodeling, and right ventricular hypertrophy, and increased alveolar and vascular development. See the article on page 863.