HIF1A and acute respiratory distress syndrome: Albeit we lack a direct proof, it is tempting to speculate that the hyperoxia-related attenuation of pulmonary and systemic inflammation was due to down-regulation of HIF-1α expression: Both genetic deletion [69,70] and pharmacological blockade [71] of HIF-1α attenuated the local and systemic inflammatory response and thereby reduced the severity of ALI after remote [69,70] or direct [71] organ damage.