Lung fibrosis has a distinct point in idiopathic pulmonary fibrosis from the renin-angiotensin pathway. this system is reported in many works of literature to share many immune/inflammatory responses to lung damage. Most importantly, the Inhibition of ACE2 was shown to enhance the level of Ang II peptides which is a ligand for type 1 angiotensin receptor (AT1R) and is considered one of the risk factors for lung fibrosis. vasoconstriction, endothelial dysfunction, and cell death. The renin-angiotensin system plays a critical role in the fibrogenesis and inflammation damage of many organs. The inhibition of ACE-2 has shown promising potential in the Molecular initiation event which leading to pulmonary fibrosis. This AOP describes the role of ACE-2 in fibrotic damage of the lung as an adverse outcome through the fibrogenic components, proinflammatory cytokines, and oxygen deficiency.
ACE2 is an essential enzyme of blood pressure regulation in the renin-angiotensin system. Angiotensin-converting enzyme (ACE) synthesizes the dominant vasoconstriction, inflammatory and profibrotic angiotensin II (Ang II) through its carboxypeptidase function on the decapeptide angiotensin I. In the meantime, Angiotensin-converting enzyme 2 (ACE2) is an exopeptidase that catalyzes the conversion of angiotensin Il to the conversion of angiotensin 1-7 function as vasodilation, anti-inflammation and anti-fibrotic. This AOP describes the dysfunction of ACE2, which results in a high level of angiotensin Ang II synthesized by ACE, which can further lead to pulmonary fibrosis by excessive collagen deposition and interact with TGF beta as the most potent profibrotic factor.