Abstract:novel coronavirus (2019-nCoV) invades cells with angiotensin converting enzyme 2 (ACE2) as a receptor to cause infection, and the result of “cytokine storm” is the significant reason inducing coronavirus disease 2019 (COVID-19)s outbreak and death. Clinical data shows that 2019-nCoV is not only involved in the respiratory system, but also accompanied by heart injury, such as acute myocardial injury, arrhythmia and fulminant myocarditis. This review mainly describes the main manifestations, mechanism and prevention strategies of heart injury caused by 2019-nCoV.

Abstract:The 2019 novel coronavirus (2019-nCoV) was discovered in an unidentified viral pneumonia case in Wuhan, China in December 2019, and was named by the World Health Organization (WHO) on January 2,0. The disease caused by 2019-nCoV was named corona virus disease 2019 by WHO on February 2,0. Recent studies have shown that angiotensin converting enzyme 2 (ACE2) is likely to be a mediating receptor of 2019-nCoV-infected cells, and ACE2 is mostly expressed in type Ⅱ alveolar cells in the human lung cells. The high expression of ACE2 in type Ⅱ alveolar cells may explain acute respiratory distress syndrome (ARDS) after 2019-nCoV infection. The first completed pathologic dissection of a patient who died of 2019-nCoV-pneumonia revealed diffuse alveolar injury and lung transparent membrane formation, consistent with ARDS.

Abstract:Since December 2019, corona virus disease 2019 (COVID-19) infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) break out, and the outbreak has spread rapidly all over the world. In addition to respiratory symptoms, COVID-19 has damage to the cardiovascular system in some cases. And the patients with underlying cardiovascular diseases lead to increased mortality. SARS-CoV-2 belongs to the family of coronaviridae, subfamily coronovirinae, β-coronavirus. The sequence identity between SARS-CoV-2 and SARS coronavirus (SARS-CoV) has 79.5% homology, and SARS-CoV-2 uses the same cell entry receptor, receptor angiotensin-converting enzyme 2 (ACE2), as SARS-CoV. The type Ⅱ alveolar cells expressing ACE2 are the main target cells for SARS-CoV-2. Therefore, it is of great significance to understand the cardiovascular system damage caused by SARS-CoV-2 and its related mechanism for the development of SARS-CoV-2 vaccine and drug and the reduction of mortality.

Abstract:Aim To investigate the effect of transfection of recombinant adenovirus vector carrying angiotensin converting enzyme 2 (ACE2) gene (Ad-ACE2) on protecting endothelium, improving insulin resistance and inhibiting liver fibrosis in apolipoprotein E knock-out (ApoE-/-) mice fed with high-fat diet. Methods ApoE-/- mice were fed with high-fat and high-energy food to simulate metabolic syndrome. 30 ApoE-/- mice were randomly divided into control group (Con group), adenovirus empty vector group (EGFP group) and ACE2 gene therapy group (ACE2 group), with 10 mice in each group, and each group was given a high-fat diet. The 3 groups were injected respectively with normal saline, Ad-EGFP and Ad-ACE2 by intravenous injection of the tail vein. At the end of 12 weeks, glucose tolerance test and insulin tolerance test were carried out. After the mice anaesthesia, blood was extracted from heart tip and blood lipid level was measured. Liver tissue was taken with HE staining and oil red O staining. Immunohistochemical staining was used to observe the expressions of ACE2, collagen-Ⅰ (COL-Ⅰ), collagen-Ⅲ (COL-Ⅲ) and interleukin-6 (IL-6) in liver tissue. Results In ACE2 group, Ad-ACE2 transfection significantly increased the expression of ACE2 in ApoE-/- mice liver (P＜0.05). The endothelium-dependent function in ACE2 group was significantly better than that in Con group and EGFP group (P＜0.05), and insulin sensitivity was stronger than that in Con group and EGFP group (P＜0.05), but the level of blood lipid did not change significantly. The COL-Ⅰ, COL-Ⅲ and IL-6 expressions of liver tissue in ACE2 group were lower than those in Con group and EGFP group (P＜0.05). Conclusion ACE2 overexpression can protect the endothelium, improve insulin resistance, inhibit liver fibrosis and thus protect liver function.