This study investigates the effects of chronic blockade of VEGF receptors on lung emphysema in rats. The researchers hypothesized that inhibiting VEGF receptors could induce alveolar cell apoptosis and lead to emphysema. They used the VEGF receptor blocker SU5416 to treat rats, which resulted in enlarged airspaces and emphysema. The treatment did not inhibit lung cell proliferation but increased alveolar septal cell apoptosis. Angiograms showed a reduction in the number of peripheral pulmonary arteries in SU5416-treated rats. Caspase 3-like activity increased in the lungs of SU5416-treated rats, indicating apoptosis. The addition of a caspase inhibitor prevented the development of emphysema and reduced alveolar cell apoptosis. The study suggests that VEGF receptor signaling is crucial for maintaining alveolar structures, and that alveolar septal cell apoptosis contributes to the pathogenesis of emphysema.This study investigates the effects of chronic blockade of VEGF receptors on lung emphysema in rats. The researchers hypothesized that inhibiting VEGF receptors could induce alveolar cell apoptosis and lead to emphysema. They used the VEGF receptor blocker SU5416 to treat rats, which resulted in enlarged airspaces and emphysema. The treatment did not inhibit lung cell proliferation but increased alveolar septal cell apoptosis. Angiograms showed a reduction in the number of peripheral pulmonary arteries in SU5416-treated rats. Caspase 3-like activity increased in the lungs of SU5416-treated rats, indicating apoptosis. The addition of a caspase inhibitor prevented the development of emphysema and reduced alveolar cell apoptosis. The study suggests that VEGF receptor signaling is crucial for maintaining alveolar structures, and that alveolar septal cell apoptosis contributes to the pathogenesis of emphysema.