FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3025101265> ?p ?o ?g. }

• W3025101265 endingPage "642" @default.
• W3025101265 startingPage "641" @default.
• W3025101265 abstract "We read the article by Agarwal et al1Agarwal A. Chen A. Ravindran N. To C. Thuluvath P.J. Gastrointestinal and liver manifestations of COVID-19.J Clin Exp Hepatol. 2020; 10: 263-265Abstract Full Text Full Text PDF PubMed Scopus (67) Google Scholar with great interest about the liver injury in coronavirus disease 2019 (COVID-19). The precise mechanism of liver injury is still unclear. These abnormalities could be due to virus-related cytopathic effects or nonviral causes such as cytokine storm, hypoxia, and hepatotoxic medications2Zhang C. Shi L. Wang F.S. Liver injury in COVID-19: management and challenges.Lancet Gastroenterol Hepatol. 2020; 5: 428-430Abstract Full Text Full Text PDF PubMed Scopus (1241) Google Scholar (Figure 1). There are no peer-reviewed published research articles on the pathogenesis of liver injury, and the pandemic has led to an unprecedented surge in preprint publications on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We sought relevant scientific studies regarding liver injury by the SARS-CoV-2 virus in four public preprint repositories (i.e., medRxiv, bioRxiv, arXiv, and Social Science Research Network). Three preliminary scientific articles explored the mechanisms of liver injury in SARS-CoV-2 infection. SARS-CoV-2 enters cells through angiotensin-converting enzyme–related carboxypeptidase (ACE2) receptors and is facilitated by transmembrane serine protease 2 (TMPRSS2). Single sequence RNA-sequencing (RNA-seq) data in healthy liver tissues from two independent cohorts demonstrated that ACE2 is mainly expressed on cholangiocytes (59.7%) but not in hepatocytes (2.6%).3Chai X. Hu L. Zhang Y. et al.Specific ACE2 expression in cholangiocytes may cause liver damage after 2019-ncov infection.bioRxiv. 2020; https://doi.org/10.1101/2020.02.03.931766Crossref Scopus (0) Google Scholar Besides, the highest levels of ACE2 and TMPRSS2 were coexpressed in TROP2high cholangiocyte–biased progenitor cells of the liver.4Seow J.J.W. Pai R. Mishra A. et al.scRNA-seq reveals ACE2 and TMPRSS2 expression in TROP2+ Liver Progenitor Cells: Implications in COVID-19 associated Liver Dysfunction.bioRxiv. 2020; Google Scholar Conversely, these studies did not explore specific mechanisms of cholangiocyte injury, ACE2 independent hepatocyte infection, and intrinsic antiviral responses. The results suggest that SARS-CoV-2 infection of the cholangiocytes and progenitor cell population might compromise the regenerative capabilities of the liver. Furthermore, Guan et al5Guan G.W. Gao L. Wang J.W. et al.Exploring the mechanism of liver enzyme abnormalities in patients with novel coronavirus-infected pneumonia.Zhonghua Gan Zang Bing Za Zhi. 2020; ([Epub ahead of print])https://doi.org/10.3760/cma.j.issn.1007-3418.2020.02.002Crossref PubMed Scopus (113) Google Scholar explored the expression changes of ACE2 and performed RNA-seq analysis of gene expression changes in the liver remnant of the hepatectomy mouse model at different time points. mRNA levels of ACE2 were upregulated during maximum hepatocyte proliferation and returned to normal with the stoppage of hepatocyte regeneration. In addition, TROP2 protein expression was upregulated explicitly in mouse and rat injury models with oval cell activation.6Okabe M. Tsukahara Tanaka M. et al.Potential hepatic stem cells reside in EpCAM+ cells of normal and injured mouse liver.Development. 2009; 136: 1951-1960Crossref PubMed Scopus (234) Google Scholar The authors hypothesized that the ACE2 expression on cholangiocytes might have retained on some of the neohepatocytes during liver regeneration after hepatic injury, and these neohepatocytes are susceptible to SARS-CoV-2 infection. Another study explored the mechanisms of liver injury SARS-CoV-2 infection of cholangiocytes in a human liver ductal organoid model.7Zhao B. Ni C. Gao R. et al.Recapitulation of SARS-CoV-2 Infection and Cholangiocyte Damage with Human Liver Organoids.bioRxiv. 2020; Google Scholar The cholangiocytes in the model were permissible for SARS-CoV-2 infection and supported the viral replication. The infection also ablated the tight junction protein, claudin 1, and significantly reduced the expression of bile acid transporters, apical sodium-dependent bile acid transporters (ASBT), and cystic fibrosis transmembrane conductance regulators (CFTR). These changes in cholangiocytes could be due to the modulation of gene expression by SARS-CoV-2 infection. The study suggests that the liver injury in COVID-19 might be partly due to direct injury of cholangiocytes and subsequent accumulation of bile acids by the SARS-CoV-2 infection. The temporary damage of hepatocytes by nonviral causes usually restored by liver regeneration and infection of cholangiocyte precursor cells might impair liver regeneration in COVID-19, leading to further deterioration of liver function. In summary, the preliminary studies suggest that the strong predilection for cholangiocyte infection and consequently impaired liver regeneration might be responsible for liver injury in COVID-19. The authors have none to declare. None." @default.
• W3025101265 created "2020-05-21" @default.
• W3025101265 creator A5019022531 @default.
• W3025101265 creator A5030804963 @default.
• W3025101265 creator A5055799027 @default.
• W3025101265 creator A5062210742 @default.
• W3025101265 date "2020-11-01" @default.
• W3025101265 modified "2023-10-11" @default.
• W3025101265 title "Pathogenesis of Liver Injury in Coronavirus Disease 2019" @default.
• W3025101265 cites W2122114596 @default.
• W3025101265 cites W3010637630 @default.
• W3025101265 cites W3013536320 @default.
• W3025101265 doi "https://doi.org/10.1016/j.jceh.2020.05.006" @default.
• W3025101265 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7237376" @default.
• W3025101265 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32837092" @default.
• W3025101265 hasPublicationYear "2020" @default.
• W3025101265 type Work @default.
• W3025101265 sameAs 3025101265 @default.
• W3025101265 citedByCount "24" @default.
• W3025101265 countsByYear W30251012652020 @default.
• W3025101265 countsByYear W30251012652021 @default.
• W3025101265 countsByYear W30251012652022 @default.
• W3025101265 countsByYear W30251012652023 @default.
• W3025101265 crossrefType "journal-article" @default.
• W3025101265 hasAuthorship W3025101265A5019022531 @default.
• W3025101265 hasAuthorship W3025101265A5030804963 @default.
• W3025101265 hasAuthorship W3025101265A5055799027 @default.
• W3025101265 hasAuthorship W3025101265A5062210742 @default.
• W3025101265 hasBestOaLocation W30251012651 @default.
• W3025101265 hasConcept C126322002 @default.
• W3025101265 hasConcept C142724271 @default.
• W3025101265 hasConcept C159047783 @default.
• W3025101265 hasConcept C203014093 @default.
• W3025101265 hasConcept C2776637226 @default.
• W3025101265 hasConcept C2777648638 @default.
• W3025101265 hasConcept C2779134260 @default.
• W3025101265 hasConcept C2779559532 @default.
• W3025101265 hasConcept C2780942790 @default.
• W3025101265 hasConcept C3008058167 @default.
• W3025101265 hasConcept C524204448 @default.
• W3025101265 hasConcept C71924100 @default.
• W3025101265 hasConceptScore W3025101265C126322002 @default.
• W3025101265 hasConceptScore W3025101265C142724271 @default.
• W3025101265 hasConceptScore W3025101265C159047783 @default.
• W3025101265 hasConceptScore W3025101265C203014093 @default.
• W3025101265 hasConceptScore W3025101265C2776637226 @default.
• W3025101265 hasConceptScore W3025101265C2777648638 @default.
• W3025101265 hasConceptScore W3025101265C2779134260 @default.
• W3025101265 hasConceptScore W3025101265C2779559532 @default.
• W3025101265 hasConceptScore W3025101265C2780942790 @default.
• W3025101265 hasConceptScore W3025101265C3008058167 @default.
• W3025101265 hasConceptScore W3025101265C524204448 @default.
• W3025101265 hasConceptScore W3025101265C71924100 @default.
• W3025101265 hasIssue "6" @default.
• W3025101265 hasLocation W30251012651 @default.
• W3025101265 hasLocation W30251012652 @default.
• W3025101265 hasOpenAccess W3025101265 @default.
• W3025101265 hasPrimaryLocation W30251012651 @default.
• W3025101265 hasRelatedWork W2031436792 @default.
• W3025101265 hasRelatedWork W2044069055 @default.
• W3025101265 hasRelatedWork W2075226651 @default.
• W3025101265 hasRelatedWork W2354901326 @default.
• W3025101265 hasRelatedWork W2389269289 @default.
• W3025101265 hasRelatedWork W3032540778 @default.
• W3025101265 hasRelatedWork W3094613772 @default.
• W3025101265 hasRelatedWork W3133874039 @default.
• W3025101265 hasRelatedWork W3137883678 @default.
• W3025101265 hasRelatedWork W4285138920 @default.
• W3025101265 hasVolume "10" @default.
• W3025101265 isParatext "false" @default.
• W3025101265 isRetracted "false" @default.
• W3025101265 magId "3025101265" @default.
• W3025101265 workType "article" @default.