Targeted Expression of Heme Oxygenase-1 and Pulmonary Responses to Hypoxia

Acute hypoxia in the lung causes arteriolar vasoconstriction whereas prolonged hypoxia promotes proliferation and migration of vascular smooth muscle cells (VSMC) and extracellular matrix deposition in the arterial wall, a process known as vascular remodeling.1 These abnormalities are characteristic of pulmonary hypertension.2 Several clinical conditions characterized by lung inflammation have been linked to the development of chronic pulmonary hypertension.3 Interestingly, perivascular inflammatory cell infiltration as well as increased serum levels of pro-inflammatory cytokines, such as interleukin (IL)-lβ and IL-6, have been reported in clinical cases of primary pulmonary hypertension.4-5 However, little attention has been given up to now to the role of pulmonary inflammation in the pathogenesis of pulmonary hypertension induced by hypoxia.