Features and Applications of Angiotensin I Converting Enzyme 2

Angiotensin-converting enzyme 2 (ACE2) is a member of the renin-angiotensin system (RAS). It is a pleiotropic monocarboxypeptidase with high homology to ACE, but ACE2 has the opposite effect of ACE. The ACE2 gene is located on chromosome Xp22 (5) and contains 18 exons. ACE2 is a zinc ion-dependent metalloprote consisting of 805 amino acids. ACE2 is consistent with the distribution of ACE, and it plays a role in the negative regulation of RAS system in vivo. Most tissues in the ACE distribution have a distribution of ACE2, such as heart, kidney, testis, placenta, colon, and small intestine. However, compared with ACE, ACE2 mRNA expression is not as extensive as ACE. It has high tissue specificity, mainly distributed in coronary artery, renal vascular endothelium, and renal tubular endothelium.

ACE2 is an extremely critical regulator of cardiac function. ACE2 knockout mice have severe cardiac dysfunction, mainly characterized by thinning of the left ventricle and decreased systolic function. This reveals that the ACE2-Ang(1-7)-Mas axis plays a role in the physiological processes of the heart. Studies have shown that overexpression of ACE2 can also regulate the imbalance of MMPs/TIMPs system and reduce the expression of the fibrosis index of transforming growth factor-? (TGF-?) and its marker? smooth muscle actin (smooth muscle actin-?,?-SMA). At the same time, it will also reduce AngII, increase the expression of Ang (1-7), make the RAS system balance to the protective direction, and improve myocardial hypertrophy and myocardial remodeling. Therefore, ACE2 is achieved by converting AngII to Ang (1-7), and Ang (1-7) directly acts on fibroblasts of the myocardium to achieve myocardial remodeling by balancing MMPs/TIMPs.

As a key enzyme in the RAS system, ACE2 is highly expressed in various parts of the kidney. In the human renal tubules, glomerular visceral epithelial cells and parietal epithelial cells, vascular smooth muscle cells, interlobular artery endothelial cells have ACE2 distribution, and actively participate in the physiological and pathological processes of the kidney. In the kidney of ACE2 gene-deficient rats, AngII increased significantly. As a result, fibrous collagen deposition increased and glomerular sclerosis occurred early. The kidneys of the mice were excised for 4 weeks while an angiotensin receptor blocker (ARB) drug was used as a control. Renal injury and proteinuria were exacerbated by the use of the ACE2 inhibitor LMN-4760 alone or in combination with ARB without changing blood pressure. This reveals that ACE2 has a protective effect on early chronic kidney disease.

As a key enzyme in the RAS system, ACE2 is highly expressed in various parts of the kidney. In the human renal tubules, glomerular visceral epithelial cells and parietal epithelial cells, vascular smooth muscle cells, interlobular artery endothelial cells have ACE2 distribution, and actively participate in the physiological and pathological processes of the kidney. In the kidney of ACE2 gene-deficient rats, AngII increased significantly. As a result, fibrous collagen deposition increased and glomerular sclerosis occurred early. The kidneys of the mice were excised for 4 weeks while an angiotensin receptor blocker (ARB) drug was used as a control. Renal injury and proteinuria were exacerbated by the use of the ACE2 inhibitor LMN-4760 alone or in combination with ARB without changing blood pressure. This reveals that ACE2 has a protective effect on early chronic kidney disease.

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