Bronchopulmonary dysplasia (BPD) is a chronic lung disease that occurs in premature infants who have needed mechanical ventilation and oxygen therapy. BPD is defined as the presence of persistent respiratory symptoms, the need for supplemental oxygen to treat hypoxemia, and an abnormal chest radiograph at 36 weeks gestational age. Proinflammatory cytokines and altered angiogenic gene signaling impair prenatal and postnatal lung growth, resulting in BPD. Postnatal hyperoxia exposure further increases the production of cytotoxic free radicals, which cause lung injury and increase the levels of proinflammatory cytokines. Magnesium is the fourth most abundant metal in the body. It is commonly used for the treatment of preeclamsia, as well as for premature labor alleviation. Magnesium's role in BPD development is not clear. A significant association between high magnesium levels at birth and respiratory distress syndrome (RDS), pulmonary interstitial emphysema in the extremely low birth weight, respiratory failure, and later development BPD was found. Conversely, low magnesium intake is associated with lower lung functions, and hypomagnesemia was found in 16% of patients with acute pulmonary diseases. Magnesium is used for the treatment of asthmatic attacks. Magnesium deficiency in pregnant women is frequently seen due to low intake. Hypomagnesemia was also found among preterm neonates and respiratory distress syndrome (RDS). Experimental hypomagnesemia evokes an inflammatory response, and oxidative damage of tissues. These were accompanied by changes in gene expression mostly involved in regulation of cell cycle, apoptosis and remodeling, processes associated with BPD. It is rational to believe that hypomagnesemia can contribute to BPD pathogenesis.