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Editorial
. 2021 Sep;75(3):503-505.
doi: 10.1016/j.jhep.2021.07.008. Epub 2021 Jul 15.

Unraveling the role of liver sinusoidal endothelial cells in COVID-19 liver injury

Affiliations
Editorial

Unraveling the role of liver sinusoidal endothelial cells in COVID-19 liver injury

Antonio Saviano et al. J Hepatol. 2021 Sep.
No abstract available

Keywords: COVID-19; Liver sinusoidal endothelial cells; SARS-CoV-2; interleukin-6; liver injury.

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Conflict of interest statement

Conflict of interest The authors do not declare any conflict of interest.

Figures

Fig. 1
Fig. 1
Model of LSEC activation and cellular crosstalk during COVID-19 according to McConnell, Kawaguchi et al. SARS-CoV-2 infection induces a systemic release of IL-6 which activates LSECs via a trans-signaling pathway involving the sIL-6R and gp130. Activated LSECs acquire a procoagulant and proinflammatory phenotype, secrete vWF, Factor VIII, CXCL1 and 2 and cell adhesion molecules ultimately favoring platelet aggregation and neutrophil recruitment in the liver. Moreover, LSECs produce IL-6 and cross talk with hepatocytes, which respond to IL-6 via a classical signaling pathway involving the IL-6R. Hepatocytes contribute to the systemic response to SARS-CoV2 infection by producing fibrinogen and acute phase proteins. Gp130, glycoprotein 130; IL-6, interleukin-6; IL-6R, interleukin 6 receptor; LSECs, liver sinusoidal endothelial cells; sIL-6R, soluble interleukin 6 receptor; vWF, von Willebrand factor.

Comment on

  • Liver injury in COVID-19 and IL-6 trans-signaling-induced endotheliopathy.
    McConnell MJ, Kawaguchi N, Kondo R, Sonzogni A, Licini L, Valle C, Bonaffini PA, Sironi S, Alessio MG, Previtali G, Seghezzi M, Zhang X, Lee AI, Pine AB, Chun HJ, Zhang X, Fernandez-Hernando C, Qing H, Wang A, Price C, Sun Z, Utsumi T, Hwa J, Strazzabosco M, Iwakiri Y. McConnell MJ, et al. J Hepatol. 2021 Sep;75(3):647-658. doi: 10.1016/j.jhep.2021.04.050. Epub 2021 May 13. J Hepatol. 2021. PMID: 33991637 Free PMC article.

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