Imai and colleagues [37] demonstrated the role of ACE2 in ARDS pathogenesis. They found that a more severe ARDS was reached in ACE2 knockout mice, and this phenotype was reversed by double genetic deletion of the ACE2 and ACE genes or by the treatment with recombinant human ACE2 (rhACE2). Furthermore, Ang II levels were related International Journal of Hypertension to the severity of the lung injury. Of note, ACE2 is widely expressed in the pulmonary endothelium, vasculature, and pneumocytes [119, 120] . Also, rhACE2 inhibited the increase of Ang II and TNF-α levels, attenuated the arterial hypoxemia and PH, and ameliorated the distribution of the pulmonary blood flow in lipopolysaccharide-induced lung injury in piglets [121] . Therefore, these studies suggest that ACE2 is a suitable target to arrest the development of ARDS in patients at risk.