WP5035 - ACE2 inhibition leads to pulmonary fibrosis - Homo sapiens

This AOP outlines how ACE-2 plays a detrimental role in causing fibrotic damage to the lung by influencing various factors such as fibrogenic components, proinflammatory cytokines, and a lack of oxygen. When the activity of ACE2 is suppressed, the conversion of Ang II into Ang-(1-7) is not properly facilitated. Consequently, the levels of proinflammatory Ang II rise, while the levels of anti-inflammatory Ang-(1-7) decrease. Notably, ACE2 inhibition has been observed to raise the levels of Ang II peptides, which are a ligand for the type 1 angiotensin receptor (AT1R). This phenomenon is considered a significant risk factor for lung fibrosis, vasoconstriction, endothelial dysfunction, and cell death.