Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
, 23 (43), 7666-7677

Pathological Process of Liver Sinusoidal Endothelial Cells in Liver Diseases

Affiliations
Review

Pathological Process of Liver Sinusoidal Endothelial Cells in Liver Diseases

Yao Ni et al. World J Gastroenterol.

Abstract

Cirrhosis develops from liver fibrosis and is the severe pathological stage of all chronic liver injury. Cirrhosis caused by hepatitis B virus and hepatitis C virus infection is especially common. Liver fibrosis and cirrhosis involve excess production of extracellular matrix, which is closely related to liver sinusoidal endothelial cells (LSECs). Damaged LSECs can synthesize transforming growth factor-beta and platelet-derived growth factor, which activate hepatic stellate cells and facilitate the synthesis of extracellular matrix. Herein, we highlight the angiogenic cytokines of LSECs related to liver fibrosis and cirrhosis at different stages and focus on the formation and development of liver fibrosis and cirrhosis. Inhibition of LSEC angiogenesis and antiangiogenic therapy are described in detail. Targeting LSECs has high therapeutic potential for liver diseases. Further understanding of the mechanism of action will provide stronger evidence for the development of anti-LSEC drugs and new directions for diagnosis and treatment of liver diseases.

Keywords: Cirrhosis; Fibrosis; Hepatitis; Liver disease; Sinusoidal endothelial cells.

Conflict of interest statement

Conflict-of-interest statement: The authors declare no conflict of interests related to this article.

Figures

Figure 1
Figure 1
Morphological changes of liver sinusoidal endothelial cells. A: TEM image of rat liver sinusoid after transversal cut; B: SEM image of rat liver sinusoid; C: AFM image of LSECs with a 10 nm gold layer; D: A high scan range of AFM image of LSECs. A-B: ref 21 Copyright @1985 by the American Association for the Study of Liver Diseases; C-D: ref 22 Copyright @ 2012 Elsevier Ltd. AFM: Atomic force microscopy; LSECs: Liver sinusoidal endothelial cells; SEM: Scanning electron microscopy; TEM: Transmission electron microscopy.
Figure 2
Figure 2
Pathological changes of hepatocytes after infection. A: Histopathological analysis was conducted on livers from mock-infected and virus-infected mice from each group at 24 and 72 h after infection; B: Summary of occurrence of necrotic and virus-infected mice at 24, 48 and 72 h after infection. A-B: ref 41 Copyright @ 2016 American Society for Microbiology.
Figure 3
Figure 3
Scanning electron microscopy of liver sinusoidal endothelial cells sieve plates in CCl4-induced liver fibrosis. A: Control group; B: CCl4 group; C: TMP- (100 mg/kg) and CCl4-treated group; D: Imatinib- (10 mg/kg) and CCl4-treated group. Scale bar = 1 μm. A-D: Ref 54 Copyright @ 2017 International Union of Biochemistry and Molecular Biology. CCl4: Carbon tetrachloride; TMP: Tetramethylpyrazine.
Figure 4
Figure 4
Relationship between liver sinusoidal endothelial cells and liver regeneration. A: Strategy to test liver regeneration in mice lacking HDL-S1P; B: Ultrastructure of LSECs in control and test groups after PH (dashed line represents increased LSEC-hepatocyte distance; inset shows higher level of perivascular matrix protein, black arrows and red arrowheads indicate the borders of LSECs and hepatocytes). Scale bar = 5 μm. A-B: ref 60 Copyright @ 2016 American Society for Clinical Investigation. HDL: High-density lipoprotein; LSECs: Liver sinusoidal endothelial cells; PH: Partial hepatectomy.
Figure 5
Figure 5
Ultrastructural localization of PTRF and SDPR in cirrhotic tissue. A: Immunogold particles suggesting PTRF expression was observed on caveola-like structures in capillarized, longitudinally cut LSECs; B: Immunogold particles suggesting SDPR expression on caveola-like structures in longitudinally cut LSECs (inset shows lower magnification; white arrowheads indicate caveola-like structures). A-B: ref 66 Copyright @ 2015 Elsevier Ltd. LSECs: Liver sinusoidal endothelial cells; PTRF: Polymerase 1 and transcript release factor; SDPR: Serum deprivation protein response.

Similar articles

See all similar articles

Cited by 4 PubMed Central articles

References

    1. Le Bail B, Bioulac-Sage P, Senuita R, Quinton A, Saric J, Balabaud C. Fine structure of hepatic sinusoids and sinusoidal cells in disease. J Electron Microsc Tech. 1990;14:257–282. - PubMed
    1. Poisson J, Lemoinne S, Boulanger C, Durand F, Moreau R, Valla D, Rautou PE. Liver sinusoidal endothelial cells: Physiology and role in liver diseases. J Hepatol. 2017;66:212–227. - PubMed
    1. Breiner KM, Schaller H, Knolle PA. Endothelial cell-mediated uptake of a hepatitis B virus: a new concept of liver targeting of hepatotropic microorganisms. Hepatology. 2001;34:803–808. - PubMed
    1. Pöhlmann S, Zhang J, Baribaud F, Chen Z, Leslie GJ, Lin G, Granelli-Piperno A, Doms RW, Rice CM, McKeating JA. Hepatitis C virus glycoproteins interact with DC-SIGN and DC-SIGNR. J Virol. 2003;77:4070–4080. - PMC - PubMed
    1. Broering R, Wu J, Meng Z, Hilgard P, Lu M, Trippler M, Szczeponek A, Gerken G, Schlaak JF. Toll-like receptor-stimulated non-parenchymal liver cells can regulate hepatitis C virus replication. J Hepatol. 2008;48:914–922. - PubMed

MeSH terms

Feedback