tetano
Editor, Senior Moderator
Am J Physiol Cell Physiol
. 2022 Feb 9.
doi: 10.1152/ajpcell.00169.2021. Online ahead of print.
The atlas of ACE2 expression in fetal and adult human hearts reveals the potential mechanism of heart injured patients infected with SARS-CoV-2
Xiuli Shao[SUP] 1 [/SUP], Xiaolin Zhang[SUP] 1 [/SUP], Ruijia Zhang[SUP] 1 [/SUP], Rongli Zhu[SUP] 1 [/SUP], Xiuyang Hou[SUP] 1 [/SUP], Weijue Yi[SUP] 1 [/SUP], Fengmin Wu[SUP] 1 [/SUP], Liying Hao[SUP] 1 [/SUP], Rui Feng[SUP] 1 [/SUP]
Affiliations
Abstract
Numerous studies have shown that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect host cells through binding to Angiotensin I Converting Enzyme 2 (ACE2) expressing in various tissues and organs. In this study, we deeply analyzed the single-cell expression profiles of ACE2 in fetal and adult human hearts to explore the potential mechanism of SARS-CoV-2 harming the heart. The molecular docking software was used to simulate the binding of SARS-CoV-2 spike protein with ACE2. The genes closely related to ACE2 in renin-angiotensin system (RAS) were identified by constructing a protein-protein interaction network. Through the analysis of single-cell transcription profiles at different stages of human embryos, we found that the expression level of ACE2 in ventricular myocytes was increased with embryonic development. The results of single-cell sequencing analysis showed that the expression of ACE2 in ventricular myocytes was up-regulated in heart failure induced by dilated cardiomyopathy compared with normal hearts. The up-regulation of ACE2 increases the risk of infection with SARS-CoV-2 in fetal and adult human hearts. In addition, the pathway analysis revealed that ACE2 may regulate the differently expressed genes in heart failure through calcium signaling pathway and Wnt signaling pathway.
Keywords: ACE2; RAS system; SARS-CoV-2; embryonic development; heart failure.
. 2022 Feb 9.
doi: 10.1152/ajpcell.00169.2021. Online ahead of print.
The atlas of ACE2 expression in fetal and adult human hearts reveals the potential mechanism of heart injured patients infected with SARS-CoV-2
Xiuli Shao[SUP] 1 [/SUP], Xiaolin Zhang[SUP] 1 [/SUP], Ruijia Zhang[SUP] 1 [/SUP], Rongli Zhu[SUP] 1 [/SUP], Xiuyang Hou[SUP] 1 [/SUP], Weijue Yi[SUP] 1 [/SUP], Fengmin Wu[SUP] 1 [/SUP], Liying Hao[SUP] 1 [/SUP], Rui Feng[SUP] 1 [/SUP]
Affiliations
- PMID: 35138176
- DOI: 10.1152/ajpcell.00169.2021
Abstract
Numerous studies have shown that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect host cells through binding to Angiotensin I Converting Enzyme 2 (ACE2) expressing in various tissues and organs. In this study, we deeply analyzed the single-cell expression profiles of ACE2 in fetal and adult human hearts to explore the potential mechanism of SARS-CoV-2 harming the heart. The molecular docking software was used to simulate the binding of SARS-CoV-2 spike protein with ACE2. The genes closely related to ACE2 in renin-angiotensin system (RAS) were identified by constructing a protein-protein interaction network. Through the analysis of single-cell transcription profiles at different stages of human embryos, we found that the expression level of ACE2 in ventricular myocytes was increased with embryonic development. The results of single-cell sequencing analysis showed that the expression of ACE2 in ventricular myocytes was up-regulated in heart failure induced by dilated cardiomyopathy compared with normal hearts. The up-regulation of ACE2 increases the risk of infection with SARS-CoV-2 in fetal and adult human hearts. In addition, the pathway analysis revealed that ACE2 may regulate the differently expressed genes in heart failure through calcium signaling pathway and Wnt signaling pathway.
Keywords: ACE2; RAS system; SARS-CoV-2; embryonic development; heart failure.