Severe Acute Respiratory Syndrome Coronavirus 2 Receptor Angiotensin Converting Enzyme 2 and Its Related Intervention Drugs / 中国药学杂志

The coronavirus disease 2019 (COVID-19) outbreak is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) around the world, which has posed a great threat to global public health security. Angiotensin converting enzyme 2 (ACE2) has been identified as the major functional receptor of SARS-CoV-2, which plays an essential role in mediating virus invasion into host cells. Thus, an in-depth understanding of the recent progress of ACE2, its relationship with the virus and related drugs is of great significance for the prevention and treatment of COVID-19. Here, from the aspects of structure, expression and function, this article reviews the latest research progress of ACE2 and SARS-CoV-2. Meanwhile, this article also summarizes the mechanism of ACE2-mediated virus invasion and ACE2-related drugs, which will provide theoretical reference for viral prevention and treatment.

Angiotensin II type 1 receptor autoantibody induces myocardial fibrosis by activating cardiac fibroblasts / 生理学报

Myocardial fibrosis (MF) is an important pathological process of cardiac remodeling in patients with heart failure; however its etiology has not been clear. It has been known that the angiotensin II type 1 receptor autoantibody (AT1-AA) is present in patients with heart failure, but it is unclear whether this antibody directly causes MF. In this study, we investigated the role of AT1-AA in MF and its effects on cardiac fibroblasts (CFs). The AT1-AA positive rat model was established by active immunization method, and the measurement of indexes were made in the 8th week after active immunity. The results of heart echocardiography showed that the cardiac systolic and diastolic functions of AT1-AA positive rats were impaired with reduced left ventricular wall thickness and enlarged heart chambers. HE staining results showed that the myocardial fibers were disorganized and ruptured, and Masson staining revealed that the area of collagen fibers around the myocardium and coronary arteries was significantly increased in AT1-AA positive group compared with that of the control group (P < 0.05). Moreover, primary CFs isolated from neonatal rats were cultured and treated with AT1-AA for 48 h. CCK-8 and immunofluorescence staining results showed that AT1-AA enhanced proliferation rate of CFs (P < 0.001), and Western blot results showed that AT1-AA significantly increased expressions of collagen I (Col I), Col III, matrix metalloproteinase-2 (MMP-2) and MMP-9 in CFs (all P < 0.05). Taken together, these results suggest that AT1-AA may induce MF and cardiac dysfunction via activating CFs.