Clinical and Molecular Hepatology

"Liver sinusoidal endothelial cell"

Review

Liver fibrosis, cirrhosis, and portal hypertension

Sinusoidal communication in chronic liver disease: Albert Gibert-Ramos, María Andrés-Rozas, Raül Pastó, Pablo Alfaro-Retamero, Sergi Guixé-Muntet, Jordi Gracia-Sancho; Clin Mol Hepatol 2025;31(1):32-55.
Published online October 2, 2024; DOI: https://doi.org/10.3350/cmh.2024.0734

Abstract
PDF

The liver sinusoid, mainly composed of liver sinusoidal endothelial cells, hepatic macrophages and hepatic stellate cells, shapes the hepatic vasculature and is key to maintaining liver homeostasis and function. During chronic liver disease (CLD), the function of sinusoidal cells is impaired, being directly involved in the progression of liver fibrosis, cirrhosis, and main clinical complications including portal hypertension and hepatocellular carcinoma. In addition to their roles in liver diseases pathobiology, sinusoidal cells’ paracrine communication or cross-talk is being studied as a mechanism of disease but also as a remarkable target for treatment. The aim of this review is to gather current knowledge of intercellular signalling in the hepatic sinusoid during the progression of liver disease. We summarise studies developed in pre-clinical models of CLD, especially emphasizing those pathways characterized in human-based clinically relevant models. Finally, we describe pharmacological treatments targeting sinusoidal communication as promising options to treat CLD and its clinical complications.

Citations

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Correspondences

Liver fibrosis, cirrhosis, and portal hypertension

Correspondence to editorial on “Liver sinusoidal endothelial cell: An important yet often overlooked player in the liver fibrosis”: Jiaorong Qu, Le Wang, Xiaojiaoyang Li; Clin Mol Hepatol 2024;30(4):1002-1004.
Published online May 17, 2024; DOI: https://doi.org/10.3350/cmh.2024.0357

Citations

Citations to this article as recorded by

Liver Fibrosis: Molecular Pathogenesis and Therapeutic Interventions
Jiaorong Qu, Wenqing Qin, Minghang Dong, Zhi Ma, Si Li, Runping Liu, Ranyun Chen, Changmeng Li, Xiaojiaoyang Li
MedComm.2026;[Epub] CrossRef

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Cholestatic liver disease

Both liver parenchymal and non-parenchymal cells express JCAD protein under various circumstances: Li Xie, Li Zhang, Hui Chen, Yong-Yu Yang, Jian Wu; Clin Mol Hepatol 2024;30(2):279-280.
Published online March 20, 2024; DOI: https://doi.org/10.3350/cmh.2024.0191

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Correspondence on Letter regarding “Both liver parenchymal and non-parenchymal cells express JCAD proteins under various circumstances”
Byoung Kuk Jang
Clinical and Molecular Hepatology.2024; 30(2): 297. CrossRef

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Reviews

Liver fibrosis, cirrhosis, and portal hypertension

Liver sinusoidal endothelial cell: An important yet often overlooked player in the liver fibrosis: Jiaorong Qu, Le Wang, Yufei Li, Xiaojiaoyang Li; Clin Mol Hepatol 2024;30(3):303-325.
Published online February 28, 2024; DOI: https://doi.org/10.3350/cmh.2024.0022

Abstract
PDF

Liver sinusoidal endothelial cells (LSECs) are liver-specific endothelial cells with the highest permeability than other mammalian endothelial cells, characterized by the presence of fenestrae on their surface, the absence of diaphragms and the lack of basement membrane. Located at the interface between blood and other liver cell types, LSECs mediate the exchange of substances between the blood and the Disse space, playing a crucial role in maintaining substance circulation and homeostasis of multicellular communication. As the initial responders to chronic liver injury, the abnormal LSEC activation not only changes their own physicochemical properties but also interrupts their communication with hepatic stellate cells and hepatocytes, which collectively aggravates the process of liver fibrosis. In this review, we have comprehensively updated the various pathways by which LSECs were involved in the initiation and aggravation of liver fibrosis, including but not limited to cellular phenotypic change, the induction of capillarization, decreased permeability and regulation of intercellular communications. Additionally, the intervention effects and latest regulatory mechanisms of anti-fibrotic drugs involved in each aspect have been summarized and discussed systematically. As we studied deeper into unraveling the intricate role of LSECs in the pathophysiology of liver fibrosis, we unveil a promising horizon that pave the way for enhanced patient outcomes.

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Jiaorong Qu, Le Wang, Xiaojiaoyang Li
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Liver fibrosis, cirrhosis, and portal hypertension

Nitric oxide in liver fibrosis: The role of inducible nitric oxide synthase: Yasuko Iwakiri; Clin Mol Hepatol 2015;21(4):319-325.
Published online December 24, 2015; DOI: https://doi.org/10.3350/cmh.2015.21.4.319

Abstract
PDF

The inducible form of nitric oxide synthase (iNOS) is expressed in hepatic cells in pathological conditions. Its induction is involved in the development of liver fibrosis, and thus iNOS could be a therapeutic target for liver fibrosis. This review summarizes the role of iNOS in liver fibrosis, focusing on 1) iNOS biology, 2) iNOS-expressing liver cells, 3) iNOS-related therapeutic strategies, and 4) future directions.

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