TWIRLS, an automated topic-wise inference method based on massive literature, suggests a possible mechanism via ACE2 for the pathological changes in the human host after coronavirus infection

Xiaoyang Ji; Chunming Zhang; Yubo Zhai; Zhonghai Zhang; Chunli Zhang; Yiqing Xue; Guangming Tan; Gang Niu

It exerts most of its actions through the activation of Ang II type 1 and type 2 receptors (AT1R and AT2R) [23] . Deficiency of ACE2 causes respiratory failure pathologies such as sepsis, pneumonia, and SARS [24, 25] . It has been confirmed that genetic deletion of AT1a receptor expression can significantly improve lung function and reduce the formation of pulmonary edema compared with wild-type mice [26] . In contrast, inactivation of AT2R in mice aggravated acute lung injury. This suggests that AT1R mediates the pathogenicity of Ang II, whereas activated AT2R has a protective role [27] . Thus, ACE/AT1R and ACE2/AT2R negatively feedback to one another, playing important roles in RAS-mediated central nervous system and cardiovascular functions. The binding of the author/funder. All rights reserved. No reuse allowed without permission.