HIF1A and acute respiratory distress syndrome: Consistent with the above studies in stretched pulmonary epithelial cells in vitro, we observed that ALI-associated increases in [13C]-malate and TCA flux rates were completely abolished in mice with gene-targeted deletion of HIF1A in alveolar epithelia (Figure 10A,B), suggesting that alveolar epithelial HIF1A specifically promotes TCA flux during ALI in vivo.