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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Hypoxemia and blunted hypoxic ventilatory responses in mice lacking heme oxygenase-2.

Heme oxygenase ( HO) catalyzes physiological heme degradation and consists of two structurally related isozymes, HO-1 and HO-2. Here we show that HO-2-deficient ( HO-2(-/-)) mice exhibit hypoxemia and hypertrophy of the pulmonary venous myocardium associated with increased expression of HO-1. The hypertrophied venous myocardium may reflect adaptation to persistent hypoxemia. HO-2(-/-) mice also show attenuated ventilatory responses to hypoxia (10% O2) with normal responses to hypercapnia (10% CO2), suggesting the impaired oxygen sensing. Importantly, HO-2(-/-) mice exhibit normal breathing patterns with normal arterial CO2 tension and retain the intact alveolar architecture, thereby excluding hypoventilation and shunting as causes of hypoxemia. Instead, ventilation-perfusion mismatch is a likely cause of hypoxemia, which may be due to partial impairment of the lung chemoreception probably at pulmonary artery smooth muscle cells. We therefore propose that HO-2 is involved in oxygen sensing and responsible for the ventilation-perfusion matching that optimizes oxygenation of pulmonary blood.[1]


  1. Hypoxemia and blunted hypoxic ventilatory responses in mice lacking heme oxygenase-2. Adachi, T., Ishikawa, K., Hida, W., Matsumoto, H., Masuda, T., Date, F., Ogawa, K., Takeda, K., Furuyama, K., Zhang, Y., Kitamuro, T., Ogawa, H., Maruyama, Y., Shibahara, S. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
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