HMGB1, which was demonstrated to be crucial for viral entry

COVID‐19 prognosis is related to age and sex. The expression of ACE2 decreases with increasing age. ACE2 expression is higher in young people than in elderly individuals and higher in females than in males.11, 12 This pattern does not match the characteristic of severely ill COVID‐19 patients being mostly elderly males. We believe that whether the level of ACE2 expression is high or low is not a key factor affecting the prognosis of patients with COVID‐19. The relationship between sex and prognosis requires additional data to verify.

Despite low expression in CMs, ACE2 was highly and specifically expressed in pericytes (Figure 1E). In addition, the expression of ABCC9 and PDGFRB and the absence of MYH11 help us to reaffirm the identity of the cells as pericytes instead of SMCs (Figure 1F). Different from SMCs that are located in the coronary arteries or arterioles, pericytes spread outside the endothelial cell of capillary and part of venules, which may play an essential role in myocardial micro-circulation. This result suggested that pericyte was a potential SARS-CoV-2 virus targeted host cell type in the human heart. We further screened another two related receptors of SARS-CoV, CD209, and CLEC4M. CD209 was specifically expressed in macrophage, and co-expressed with macrophage marker gene CD163, which may enhance the virus entry in the human heart (Figure 1G). CLEC4M was not enriched in human heart cells.

Lewis male rats, 166 we found that the ARB losartan increased ACE2 activity in the heart by 2 to 3-fold as

experimental studies reveal that statins also augment the ACE2 198 expression. Tikoo et al. (45)

Northern blot analysis revealed a ≈3.4-kb ACE2 transcript expressed only in heart, kidney, and testis of 23 human tissues examined; a minor ≈8-kb band was also detected in kidney

When Ace2 is transgenically overexpressed in mouse heart, cardiac defects are again observed, most notably a lethal ventricular arrhythmia, which is associated with disruption of gap junction formation [9Donoghue M et al.Heart block, ventricular tachycardia, and sudden death in ACE2 transgenic mice with downregulated connexins.J. Mol. Cell. Cardiol. 2003; 35: 1043-1053Abstract Full Text Full Text PDF PubMed Scopus (142) Google Scholar]. The high incidence of sudden death in these mice correlated with the levels of Ace2 transgene expression. Surviving older mice showed a spontaneous downregulation of the transgene and restoration of normal cardiac function.

The mechanism of acute myocardial injury caused by SARS-CoV-2 infection might be related to ACE2. ACE2 is widely expressed not only in the lungs but also in the cardiovascular system and, therefore, ACE2-related signalling pathways might also have a role in heart injury.