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"Stellate 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
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

Citations to this article as recorded by  Crossref logo
  • Hepatic Fibrosis and Liver Cancer
    Aina Anton, Scott L. Friedman, Bruno Cogliati
    Seminars in Liver Disease.2026; 46(01): 031.     CrossRef
  • Regression of fibrosis and portal hypertension in chronic liver disease: Endothelial perspectives and clinical implications
    Yuly P Mendoza, Raül Pastó, Sonia E Selicean, Jordi Gracia-Sancho
    Annals of Hepatology.2026; 31(1): 102174.     CrossRef
  • LSEC-derived CXCL9 orchestrates immune recruitment and hepatocyte reprogramming in liver fibrosis
    Jing Li, Qiannan Di, Xiujuan Zhou, Mengling Chang, Wei Chen
    Acta Biochimica et Biophysica Sinica.2026;[Epub]     CrossRef
  • Nodular Transformation–driven Circulatory Remodeling in Biliary Atresia–induced Pediatric Biliary Cirrhosis: A Three-dimensional Phase-Contrast CT Rendering
    Bei-Ning Qi, Xin-Yan Zhao, Wen-Juan Lv, Shan Shan, Xian-qin Du, Jian-Bo Jian, Chun-Hong Hu
    Radiology.2026;[Epub]     CrossRef
  • Sinusoidal cell–derived biomarker scores predict diagnosis and prognosis in chronic liver disease
    Sergi Guixé-Muntet, Anabel Fernández-Iglesias, David Lopez, Emilio Tonina, Yiliam Fundora, Anna Zagorska, Jordi Gracia-Sancho
    BMC Medicine.2026;[Epub]     CrossRef
  • P7C3 alleviates hepatic fibrosis via targeting eIF4A1-mediated protein translation and autophagy in hepatic stellate cells
    Ailing Liang, Ling Yao, Yuanyuan Liu, Honglin He, Yao Lei, Yunheng Yang, Jun Liu, Jiamei Yu, Weiguo Cao, Zhiwei Chen
    Archives of Pharmacal Research.2026; 49(2): 262.     CrossRef
  • Clinical challenges and transjugular intrahepatic portosystemic shunt strategies for pyrrolizidine alkaloid-induced hepatic sinusoidal obstruction syndrome: an Asian perspective
    Tan-Yang Zhou, Hong-Liang Wang, Zhi-Cheng Jin, Bin Xiong, Ji Hoon Shin
    Korean Journal of Interventional Radiology.2026; 31(1): 24.     CrossRef
  • Kupffer cells and monocyte-derived macrophages in the pathogenesis and treatment of hepatocellular carcinoma
    Argyro Voumvouraki, Ioannis Tsomidis, Elias Kouroumalis
    Hepatoma Research.2026;[Epub]     CrossRef
  • Extracellular Vesicles in Hepatic Pathogenesis: From Biogenesis to Biomarkers
    Tamer A. Addissouky
    Archives of Molecular Biology and Genetics.2026; 5(1): 10.     CrossRef
  • Vasomics of the liver
    Chengyan Wang, Eric Felli, Jonathan Andrew Fallowfield, Christoph Frank Dietrich, Don Rockey, Jürgen Hennig, Gao-Jun Teng, Jordi Gracia-Sancho, Xiaolong Qi
    Gut.2025; 74(6): 1008.     CrossRef
  • Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells
    Enis Kostallari, Robert F. Schwabe, Adrien Guillot
    Cellular & Molecular Immunology.2025; 22(10): 1205.     CrossRef
  • Myeloid cells in chronic liver inflammation
    Dimitrios Patseas, Ahmed El-Masry, Zuobin Liu, Prakash Ramachandran, Evangelos Triantafyllou
    Cellular & Molecular Immunology.2025; 22(10): 1237.     CrossRef
  • Toll-like receptor 4-mediated inflammatory stimulation in Kupffer cell enhances arsenite-induced liver fibrosis by triggering hepatic stellate cell activation
    Qian Song, Meitong Zhou, Rui He, Heng Diao, Lili Fan, Chenglong Tu, Xiong Chen, Dapeng Wang
    Ecotoxicology and Environmental Safety.2025; 303: 118903.     CrossRef
  • The pathophysiological role of portal hypertension in metabolic dysfunction–associated steatotic liver disease
    Søren Møller, Sannia M.S. Sjöstedt, Lise Hobolth, Christian Mortensen, Nina Kimer
    Hepatology Communications.2025;[Epub]     CrossRef
  • Hepatocyte-derived extracellular vesicles promote endothelial dedifferentiation in chronic liver disease through the miR-153-3p-pyroptosis axis
    Laia Abad-Jordà, María Andrés-Rozas, Ana Martínez-Alcocer, Jessica Aspas, Yiliam Fundora, Sonia Fernández-Veledo, Carmen Peralta, Sergi Guixé-Muntet, Anabel Fernández-Iglesias, Jordi Gracia-Sancho
    Hepatology.2025;[Epub]     CrossRef
  • 12,480 View
  • 321 Download
  • 12 Web of Science
  • Crossref

Correspondence

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

Citations

Citations to this article as recorded by  Crossref logo
  • 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
  • 7,144 View
  • 76 Download
  • 1 Web of Science
  • Crossref

Editorial

Cholestatic liver disease

JCAD, a new potential therapeutic target in cholestatic liver disease
Byoung Kuk Jang
Clin Mol Hepatol 2024;30(2):166-167.
Published online March 8, 2024
DOI: https://doi.org/10.3350/cmh.2024.0128

Citations

Citations to this article as recorded by  Crossref logo
  • Underestimated and Overlooked Factors in PBC Progression: Bacterial and Fungal Infections
    Yaxin Zhu, Sumeng Li, Shiqi Li, Yichen Wang, Yanqin Du, Xin Zheng, Jun Wu
    International Journal of Molecular Sciences.2026; 27(6): 2766.     CrossRef
  • Breaking the metabolo-immune cycle in primary biliary cholangitis for therapeutic benefit
    Yan Song, Hui Wang, Shiyu Du, Yuqing Li, Di Yang, Min Xu, Qinglong Jin
    Frontiers in Immunology.2026;[Epub]     CrossRef
  • Both liver parenchymal and non-parenchymal cells express JCAD protein under various circumstances
    Li Xie, Li Zhang, Hui Chen, Yong-Yu Yang, Jian Wu
    Clinical and Molecular Hepatology.2024; 30(2): 279.     CrossRef
  • 8,602 View
  • 85 Download
  • 3 Web of Science
  • Crossref

Snapshot

Steatotic liver disease

Immunopathogenesis of liver fibrosis in steatotic liver disease
Chaerin Woo, Won-Il Jeong
Clin Mol Hepatol 2024;30(2):299-302.
Published online February 19, 2024
DOI: https://doi.org/10.3350/cmh.2024.0113

Citations

Citations to this article as recorded by  Crossref logo
  • Multi-target mechanisms of Banxia Baizhu Tianma Decoction against MASH in a methionine-choline deficient mouse model: insights from a Multi-Omics Investigation
    Qinying Feng, Lili Gao, Jiewen Shi, Jiekai Hua, Xiaorui Zhao, Jiankang Li, Wei Liu, Qiaoling Yang, Shuling Wang
    Journal of Ethnopharmacology.2026; 364: 121526.     CrossRef
  • Metabolic Dysfunction-Associated Steatotic Liver Disease as a Risk Factor for Chronic Kidney Disease: A Narrative Review
    Marcelo do Rego Maciel Souto Maior, Nathália de Lacerda Interaminense Ribeiro, Hannah Vicentini Vitoriano Silva, Edmundo Pessoa Lopes, Emilia Chagas Costa
    Biomedicines.2025; 13(9): 2162.     CrossRef
  • 11,415 View
  • 142 Download
  • 2 Web of Science
  • Crossref

Original Articles

Cholestatic liver disease

JCAD deficiency attenuates activation of hepatic stellate cells and cholestatic fibrosis
Li Xie, Hui Chen, Li Zhang, Yue Ma, Yuan Zhou, Yong-Yu Yang, Chang Liu, Yu-Li Wang, Ya-Jun Yan, Jia Ding, Xiao Teng, Qiang Yang, Xiu-Ping Liu, Jian Wu
Clin Mol Hepatol 2024;30(2):206-224.
Published online January 8, 2024
DOI: https://doi.org/10.3350/cmh.2023.0506
Background/Aims
Cholestatic liver diseases including primary biliary cholangitis (PBC) are associated with active hepatic fibrogenesis, which ultimately progresses to cirrhosis. Activated hepatic stellate cells (HSCs) are the main fibrogenic effectors in response to cholangiocyte damage. JCAD regulates cell proliferation and malignant transformation in nonalcoholic steatoheaptitis-associated hepatocellular carcinoma (NASH-HCC). However, its participation in cholestatic fibrosis has not been explored yet.
Methods
Serial sections of liver tissue of PBC patients were stained with immunofluorescence. Hepatic fibrosis was induced by bile duct ligation (BDL) in wild-type (WT), global JCAD knockout mice (JCAD-KO) and HSC-specific JCAD knockout mice (HSC-JCAD-KO), and evaluated by histopathology and biochemical tests. In situ-activated HSCs isolated from BDL mice were used to determine effects of JCAD on HSC activation.
Results
In consistence with staining of liver sections from PBC patients, immunofluorescent staining revealed that JCAD expression was identified in smooth muscle α-actin (α-SMA)-positive fibroblast-like cells and was significantly up-regulated in WT mice with BDL. JCAD deficiency remarkably ameliorated BDL-induced hepatic injury and fibrosis, as documented by liver hydroxyproline content, when compared to WT mice with BDL. Histopathologically, collagen deposition was dramatically reduced in both JCAD-KO and HSC-JCAD-KO mice compared to WT mice, as visualized by Trichrome staining and semi-quantitative scores. Moreover, JCAD deprivation significantly attenuated in situ HSC activation and reduced expression of fibrotic genes after BDL.
Conclusions
JCAD deficiency effectively suppressed hepatic fibrosis induced by BDL in mice, and the underlying mechanisms are largely through suppressed Hippo-YAP signaling activity in HSCs.

Citations

Citations to this article as recorded by  Crossref logo
  • Biliary YB-1/GLI2 axis facilitates ductular reaction and promotes HSC activation via SPP1/integrin αvβ1 signaling during liver fibrogenesis
    Yuecheng Guo, Qingqing Zhang, Binghang Li, Weiming Dai, Bo Shen, Zhenyang Shen, Junjun Wang, Qichao Ge, Hanjing Zhangdi, Guangwen Chen, Qidi Zhang, Xiaobo Cai, Hui Dong, Guangjian Fan, Lungen Lu, Fei Li
    Hepatology.2026; 83(6): 1365.     CrossRef
  • Features and functional mechanisms of super-enhancers in cardiovascular disorders, cancer, autoimmune diseases and neurodegenerative disorders
    Zi-Rong Li, Yong-Yan Wang, Chao Zhang, Jin-Sha Shi, Xiao Yu, Ni-Tong Ying, Xiao-Ke Xu, Juan-Juan Li, Tao Guo
    Cellular Signalling.2026; 138: 112252.     CrossRef
  • Huanggan decoction ameliorates cholestatic hepatic fibrosis in rats via TGF-β1/Smad3 signaling pathway
    Yaya Lei, Xueli Ma, Xiaohui Jin, Yanping He, Jianhong Yang, Yuna Zhao, Jing Chen, Ting Gao, Sharon DeMorrow
    PLOS One.2026; 21(3): e0344168.     CrossRef
  • Underestimated and Overlooked Factors in PBC Progression: Bacterial and Fungal Infections
    Yaxin Zhu, Sumeng Li, Shiqi Li, Yichen Wang, Yanqin Du, Xin Zheng, Jun Wu
    International Journal of Molecular Sciences.2026; 27(6): 2766.     CrossRef
  • Activated hepatic stellate cells maintain liver bile acid homeostasis through paracrine FGF10/FGFR2 signaling
    Santie Li, Gaozan Tong, Mei Xue, Leyi Shen, Kunxuan Zhu, Jianjun Feng, Junfu Fan, Junjie Lu, Xiaojing Yi, Luhai Wang, Jiaqi Liang, Weitao Cong, Xiaokun Li
    Journal of Hepatology.2026;[Epub]     CrossRef
  • Integrating Network Pharmacology and Experimental Validation to Uncover the Therapeutic Mechanisms of Chaigui Decoction in Schistosoma japonicum-Induced Liver Fibrosis
    Kaiyuan Deng, Xinyao Du, Qiao Liu, Zhi Lan, Fengning Wang, Yulin Cao, Song Xu, Xiaoli Deng, Xiang Wu, Guangjie Li, Yujiao Yang, Xin Wang, Fengyu Yang, Qingyuan Gu, Qingyang Yao, Liangzheng Zou, Wanning Wang, Mijia Yuan, Teng Zhong, Pei Huang, Yonghua Zhou
    Acta Tropica.2026; : 108160.     CrossRef
  • Transient receptor potential channel 6 knockout ameliorates hepatic fibrosis by inhibiting the activation and proliferation of hepatic stellate cells
    Xixi Zeng, Yanhong Liao, Weiyi Cheng
    Journal of Gastroenterology and Hepatology.2025; 40(1): 294.     CrossRef
  • Hepatic Stellate Cell TM4SF1 Accelerates Hepatic Fibrosis Progression via Interacting With the Tyrosine Kinase c-Src
    Shenglu Liu, Peng Tan, Jiatong Chen, Zhiwei Huang, Bingyu Ren, Zhonghao Jiang, Boyuan Gu, Wenhao Yu, Lei Sun, Yingjun Chen, Jian Ruan, Wenguang Fu
    Cellular and Molecular Gastroenterology and Hepatology.2025; 19(10): 101559.     CrossRef
  • JCAD deficiency delayed liver regenerative repair through the Hippo–YAP signalling pathway
    Li Zhang, Yong‐Yu Yang, Li Xie, Yuan Zhou, Zhenxing Zhong, Jia Ding, Zhong‐Hua Wang, Yu‐Li Wang, Xiu‐Ping Liu, Fa‐Xing Yu, Jian Wu
    Clinical and Translational Medicine.2024;[Epub]     CrossRef
  • JCAD, a new potential therapeutic target in cholestatic liver disease
    Byoung Kuk Jang
    Clinical and Molecular Hepatology.2024; 30(2): 166.     CrossRef
  • 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
  • Both liver parenchymal and non-parenchymal cells express JCAD protein under various circumstances
    Li Xie, Li Zhang, Hui Chen, Yong-Yu Yang, Jian Wu
    Clinical and Molecular Hepatology.2024; 30(2): 279.     CrossRef
  • 12,889 View
  • 301 Download
  • 10 Web of Science
  • Crossref

Cholestatic liver disease

Taurocholic acid promotes hepatic stellate cell activation via S1PR2/p38 MAPK/YAP signaling under cholestatic conditions
Jing Yang, Xujiao Tang, Zhu Liang, Mingzhu Chen, Lixin Sun
Clin Mol Hepatol 2023;29(2):465-481.
Published online February 20, 2023
DOI: https://doi.org/10.3350/cmh.2022.0327
Background/Aims
Disrupted bile acid regulation and accumulation in the liver can contribute to progressive liver damage and fibrosis. However, the effects of bile acids on the activation of hepatic stellate cells (HSCs) remain unclear. This study investigated the effects of bile acids on HSC activation during liver fibrosis, and examined the underlying mechanisms.
Methods
The immortalized HSCs, LX-2 and JS-1cells were used for the in vitro study. in vitro, the adeno-associated viruses adeno-associated virus-sh-S1PR2 and JTE-013 were used to pharmacologically inhibit the activity of S1PR2 in a murine model of fibrosis induced by a 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet. Histological and biochemical analyses were performed to study the involvement of S1PR2 in the regulation of fibrogenic factors as well as the activation properties of HSCs.
Results
S1PR2 was the predominant S1PR expressed in HSCs and was upregulated during taurocholic acid (TCA) stimulation and in cholestatic liver fibrosis mice. TCA-induced HSC proliferation, migration and contraction and extracellular matrix protein secretion were inhibited by JTE-013 and a specific shRNA targeting S1PR2 in LX-2 and JS-1 cells. Meanwhile, treatment with JTE-013 or S1PR2 deficiency significantly attenuated liver histopathological injury, collagen accumulation, and the expression of fibrogenesis-associated genes in mice fed a DDC diet. Furthermore, TCAmediated activation of HSCs through S1PR2 was closely related to the yes-associated protein (YAP) signaling pathway via p38 mitogen-activated protein kinase (p38 MAPK).
Conclusions
TCA-induced activation of the S1PR2/p38 MAPK/YAP signaling pathways plays a vital role in regulating HSC activation, which might be therapeutically relevant for targeting cholestatic liver fibrosis.

Citations

Citations to this article as recorded by  Crossref logo
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    Walaa H. El-Maadawy, Marwa Amer, Amr Mostafa, Abdelrahman A. Hassany, Nesma S. Shafie, Ahmed W. Lethy, Eman El-Ahwany, Ehab Hafiz
    International Immunopharmacology.2026; 168: 115834.     CrossRef
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Reviews

Liver fibrosis, cirrhosis, and portal hypertension

Anti-fibrotic treatments for chronic liver diseases: The present and the future
Naoshi Odagiri, Tsutomu Matsubara, Misako Sato-Matsubara, Hideki Fujii, Masaru Enomoto, Norifumi Kawada
Clin Mol Hepatol 2021;27(3):413-424.
Published online December 3, 2020
DOI: https://doi.org/10.3350/cmh.2020.0187
Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies.

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Liver fibrosis, cirrhosis, and portal hypertension

Role of cytoglobin, a novel radical scavenger, in stellate cell activation and hepatic fibrosis
Le Thi Thanh Thuy, Hoang Hai, Norifumi Kawada
Clin Mol Hepatol 2020;26(3):280-293.
Published online June 4, 2020
DOI: https://doi.org/10.3350/cmh.2020.0037
Cytoglobin (Cygb), a stellate cell-specific globin, has recently drawn attention due to its association with liver fibrosis. In the livers of both humans and rodents, Cygb is expressed only in stellate cells and can be utilized as a marker to distinguish stellate cells from hepatic fibroblast-derived myofibroblasts. Loss of Cygb accelerates liver fibrosis and cancer development in mouse models of chronic liver injury including diethylnitrosamine-induced hepatocellular carcinoma, bile duct ligation-induced cholestasis, thioacetamide-induced hepatic fibrosis, and choline-deficient L-amino acid-defined diet-induced non-alcoholic steatohepatitis. This review focuses on the history of research into the role of reactive oxygen species and nitrogen species in liver fibrosis and discusses the current perception of Cygb as a novel radical scavenger with an emphasis on its role in hepatic stellate cell activation and fibrosis.

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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

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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NADPH oxidase mediated oxidative stress in hepatic fibrogenesis
Yong-Han Paik, David A. Brenner
Korean J Hepatol 2011;17(4):251-257.
Published online December 26, 2011
DOI: https://doi.org/10.3350/kjhep.2011.17.4.251

NADPH oxidase (NOX) is a multicomponent enzyme complex that generates reactive oxygen species (ROS) in response to a wide range of stimuli. ROS is involved as key secondary messengers in numerous signaling pathways, and NADPH oxidases complex has been increasingly recognized as key elements of intracellular signaling of hepatic fibrogenesis. In the liver, NADPH oxidase is functionally expressed both in the phagocytic form and in the non-phagocytic form. The non-phagocytic NADPH oxidase complex is structurally and functionally similar to the phagocytic NADPH, resulting in reduction of molecular oxygen to generate superoxide. There are six homologous NOX proteins in the non-phagocytic forms of NADPH oxidase. An emerging concept is that both phagocytic and nonphagocytic NADPH oxidase components in hepatic stellate cells (HSCs) mediate hepatic fibrosis, suggesting its potential role as a pharmacological target for anti-fibrotic therapy. The molecular components and signaling pathways of various NADPH oxidase homologues that are critical for the fibrotic activity in HSCs need to be more clearly identified.

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The Korean Journal of Hepatology Elsewhere

The effect of sorafenib on hepatic stellate cells: implication of its effect on tumor microenvironment
Jung Il Lee
Korean J Hepatol 2010;16(4):418-419.
Published online December 31, 2010
DOI: https://doi.org/10.3350/kjhep.2010.16.4.418

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  • Sorafenib induces autophagic cell death and apoptosis in hepatic stellate cell through the JNK and Akt signaling pathways
    Huiyao Hao, Di Zhang, Junli Shi, Yan Wang, Lei Chen, Yongze Guo, Junji Ma, Xiaoyu Jiang, Huiqing Jiang
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Review

Hemodynamic alterations in cirrhosis and portal hypertension
Moon Young Kim, Soon Koo Baik, Samuel S. Lee
Korean J Hepatol 2010;16(4):347-352.
Published online December 31, 2010
DOI: https://doi.org/10.3350/kjhep.2010.16.4.347

Portal hypertension (PHT) is associated with hemodynamic changes in intrahepatic, systemic, and portosystemic collateral circulation. Increased intrahepatic resistance and hyperdynamic circulatory alterations with expansion of collateral circulation play a central role in the pathogenesis of PHT. PHT is also characterized by changes in vascular structure, termed vascular remodeling, which is an adaptive response of the vessel wall that occurs in response to chronic changes in the environment such as shear stress. Angiogenesis, the formation of new blood vessels, also occurs with PHT related in particular to the expansion of portosystemic collateral circulation. The complementary processes of vasoreactivity, vascular remodeling, and angiogenesis represent important targets for the treatment of portal hypertension. Systemic and splanchnic vasodilatation can induce hyperdynamic circulation which is related with multi-organ failure such as hepatorenal syndrome and cirrhotic cadiomyopathy.

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    Ki Tae Suk, Chang Hoon Kim, Seung Ha Park, Ho Taik Sung, Jong Young Choi, Kwang Hyub Han, So Hyung Hong, Dae Yong Kim, Jai Hoon Yoon, Yeon Soo Kim, Gwang Ho Baik, Jin Bong Kim, Dong Joon Kim
    Journal of Clinical Gastroenterology.2012; 46(10): 880.     CrossRef
  • Is there any vindication for low dose nonselective β-blocker medication in patients with liver cirrhosis?
    Tae Wan Kim, Hong Joo Kim, Chang Uk Chon, Hyun Sun Won, Jung Ho Park, Dong Il Park, Yong Kyun Cho, Chong Il Sohn, Woo Kyu Jeon, Byung Ik Kim
    Clinical and Molecular Hepatology.2012; 18(2): 203.     CrossRef
  • PPARα activation in portal hypertension
    Hongqun Liu, Samuel S. Lee, Roberto J. Groszmann, Yasuko Iwakiri, Tamar H. Taddei
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Original Article

Transcriptional profiling and Wnt signaling activation in proliferation of human hepatic stellate cells induced by PDGF-BB
HyeWon Shin, M.S., Soo Young Park, M.S., Kyoung Bun Lee, M.D., Eun Shin, M.D., Suk Woo Nam, Ph.D.1, Jung Young Lee, M.D.1, Ja-June Jang, M.D.
Korean J Hepatol 2009;15(4):486-495.
Published online December 31, 2009
DOI: https://doi.org/10.3350/kjhep.2009.15.4.486
Background/Aims
This study aimed to better understand gene expression profiles of human hepatic stellate cell (HSC) activation and the relationship with the Wnt signaling pathway. Methods: The global transcript levels in platelet derived growth factor-BB (PDGF-BB)-stimulated hTERT HSCs were analyzed using oligonucleotide microarrays. Oligonucleotide microarrays with 19K human oligo chips were performed to obtain gene expression profiles associated with proliferation in human hTERT HSCs. The microarray data was verified by real time quantitative PCR and expression of the components of Wnt signaling was analyzed by Western blot. Results: Microarray data showed 243 up-regulated and 265 down-regulated genes in PDGF-BB-treated HSCs. The changes in expression of glypican3 and BH3 interacting domain death agonist (BID) mRNA in real time quantitative PCR, especially among the highly up- or down-regulated genes, were statistically consistent with the microarray data. The Wnt signaling pathway components, frizzled10 (FZD10) and calcium/calmodulin-dependent protein kinase II alpha (CAMK2A), showed increased expression in the short time course microarray and the up-regulation of FZD10 also occurred at the protein level. Our data showed various gene expression profiles during activation of human HSC. Conclusions: The up-regulated expression of FZD10 and CAMK2A suggests that the Wnt/Ca2+ signaling pathway is active in hTERT HSCs and may participate in HSC activation and proliferation. (Korean J Hepatol 2009;15:486-495)

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    Molecular Neurobiology.2019; 56(4): 2339.     CrossRef
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    Subramaniam Puvaneswary, Hanumantharao Balaji Raghavendran, Sepehr Talebian, Malliga Raman Murali, Suhaeb A Mahmod, Simmrat Singh, Tunku Kamarul
    Scientific Reports.2016;[Epub]     CrossRef
  • Herbal medicine Gan-fu-kang downregulates Wnt/Ca2+ signaling to attenuate liver fibrogenesis in vitro and in vivo
    YUJIE JIA, LIJUN YUAN, TINGTING XU, HANSHU LI, GUANG YANG, MIAONA JIANG, CAIHUA ZHANG, CONG LI
    Molecular Medicine Reports.2016; 13(6): 4705.     CrossRef
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Review

The Role of Activated Hepatic Stellate Cells in Liver Fibrosis, Portal Hypertension and Cancer Angiogenesis
June Sung Lee , Jong Hoon Kim
Korean J Hepatol 2007;13(3):309-319.
Published online September 20, 2007
DOI: https://doi.org/10.3350/kjhep.2007.13.3.309
Although hepatic stellate cells, which are liver specific pericytes, have been recognized within the vasculature of the sinusoid for more than one hundred years, the biology and function of these cells is unclear. Recent studies have highlighted the key role of stellate cells in a number of fundamental processes that include wound healing/fibrosis, vasoregulation, and vascular remodeling/angiogenesis. In the liver, these processes are particularly important in the development of cirrhosis, portal hypertension and cancer. This article highlights the recent advances in our understanding of the biology of hepatic stellate cells and discusses some of the recently-ascribed functions that are relevant to liver fibrosis, portal hypertension and cancer angiogenesis. (Korean J Hepatol 2007;13:309-319)

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Original Articles

Protective Effect of Pentoxifylline and Ciprofloxacin on Dimethylnitrosamine-induced Hepatic Fibrosis in Rats
Kang Suek Suh,Chang Hun Lee,Mee Young Sol,Sun Kyung Lee
Korean J Hepatol 2001;7(1):34-46.
Background/Aims
Hepatic fibrosis is known to be a predisposing condition of cirrhosis for which there is no proven effective therapy. The aim of this study was to investigate the effect of pentoxifylline and ciprofloxacin on biochemical and histological features of rat hepatic fibrosis induced by dimethylnitrosamine (DMN). Methods: Seventy male Sprague-Dawley rats were divided into four groups including control (n = 10), DMN (n = 20), DMN plus pentoxifylline (n = 20) and DMN plus ciprofloxacin (n = 20). The rats were injected intraperitoneally with normal saline in the control group and the aforementioned chemicals in the study groups three times a week for 3 weeks. Two rats of the control group, and fives of each study group were sacrificed weekly after the beginning of experiment. From sacrified rats the following parameters of hepatic fibrosis were determined: AST, ALT, cytokines IL-1β, TNF-α and INF-γ, and histological features of hepatic tissue. Result: Rat weight, serological and histological findings were distinctively improved in two treated groups compared with untreated DMN group(p<0.05), The antifibrogenic activity between treated groups was rather better in the group treated with pentoxifylline than in the group treated with ciprofloxacin. During the first and second weeks after experiment the distribution of hepatic stellate cells in treated groups was limited, whereas DMN group showed their diffuse distribution. At the third week DMN group displayed micronodular cirrhosis, but treated groups showed only mild centrilobular fibrotic areas without developing cirrhosis. Conclusion: Our results indicate that pentoxifylline and cirprofloxacin may be protective against DMN induced rat hepatic fibrogenesis, while accompanying the inhibition of hepatic stellate cells during the early stage of hepatic fibrogenesis.(Korean J Hepatol 2001;7:34-46)
  • 3,179 View
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The Expression of E - cadherin in Human and Rat Hepatic Stellate Cells / Evidence of Epithelial - Mesenchymal Transition
Young Suk Lim,Hyo Suk Lee
Korean J Hepatol 2002;8(1):90-99.
Background/Aims
The embryonal origin of hepatic stellate cells (HSCs), the principal cells in hepatic fibrogenesis, is still intriguing. We have previously demonstrated that human HSCs express cytokeratins which suggests the epithelial origin of these cells. To further explore the origin and the differentiation of HSCs we studied the expression of E-cadherin, the specific marker of epithelial cells, in human and rat HSCs. Methods: We studied the changing pattern of E-cadherin expression during spontaneous activation of primarily isolated human HSCs by immunofluorescence staining and RT-PCR. To confirm the expression of E-cadherin in HSCs in vivo we performed double immunofluorescence staining for E-cadherin and glial fibrillary acidic protein, the specific identification marker of quiescent rat HSCs, in normal rat liver. Results: Quiescent human HSCs were labeled strongly by anti-E-cadherin monoclonal antibody at the first and seventh days after primary culture. Human HSCs, however, did not stain for E-cadherin after the first passage of culture. RT-PCR also confirmed these modulations of E-cadherin expression. Double immunofluorescence staining, performed on rat liver tissue and observed by confocal laser scanning microscopy, unequivocally revealed the membranous expression of E-cadherin in quiescent HSCs labeled by glial fibrillary acidic protein. Conclusions: Quiescent HSCs of humans and rats express E-cadherin both in vitro and in vivo. The extent of E-cadherin expression rapidly decreases during the process of spontaneous activation. Our results suggest that HSCs may be of epithelial origin and undergo epithelial-mesenchymal transition during activation process.(Korean J Hepatol 2002;8:90-99)
  • 3,327 View
  • 23 Download
Hepatology Elsewhere
Activated stellate cells express the TRAIL receptor-2/death receptor-5 and undergo TRAIL-mediated apoptosis. Hepatology 2003;37: 87-95
Geun Youn Gwok , Jung Hwan Yoon
Korean J Hepatol 2003;9(2):145-146.
최근 간섬유화의 resolution phase에서 활성화된 간 성상세포(hepatic stellate cell)의 수가 줄어드는 기전으로 세포사멸(apoptosis)가 중요한 역할을 담당함이 알려지고 있다. 이러한 사실은 활성화된 간 성상세포가 휴지기에 있을 때보다 세포사멸을 일으키는 자극에 더 민감하다는 것을 암시한다. 이미 다른 종류의 세포들이 휴지 상태보다 활성화된 상태에서 TRAIL (tumor necrosis factor-related apoptosis-inducing ligand)에 의한 세포사멸에 더 민감하다는 사실이 알려진 바 있기 때문에 본 연구자들은 이번 연구에서 점진적인 활성화 단계를 거치는 간 성상세포에서 단계별 TRAIL 사망 수용체(death receptor)의 발현과 TRAIL에 의한 세포 독성에 대한 민감도를 밝히고자 하였다. 자연적으로 불멸화된 인간 간 성상세포주인 LX-2 세포를 14일간 플라스틱 용기에서 배양하며 분석한 결과, 14일 후 간 성상세포 활성화의 지표인 α-smooth muscle actin (α-SMA)과 β-crystalline의 messenger RNA (mRNA)의 양이 각각 7배와 5배 증가하였으며, 같은 기간동안 TRAIL-R1/DR4와 TRAIL-R2/DR5 mRNA 발현은 각각 18배와 17.6배 증가하였다. 양적으로 보았을 때에는 TRAIL-R2/DR5의 발현이 TRAIL-R1/ DR4보다 103배 높았다. 아울러 TRAIL-R2/DR5 단백 발현과 TRAIL 유도 세포사멸에 대한 민감플라스틱 용기에서 활성화 과정을 거치는 동안 도에서도 동일한 양상의 변화가 관찰되었으며, 설치류의 간으로부터 일차배양한 간 성상세포 역시 유사한 변화를 보였다. 결론적으로 간 성상세포는 활성화되어감에 따라 TRAIL-R2/DR5 발현이 증가하고 TRAIL 유도 세포사멸에 민감해짐을 알 수 있었다. 따라서 임상적으로 TRAIL-R2/DR5 agonist가 생체 내에서 선택적으로 간 성상세포의 세포사멸을 유도하여 간섬유화를 줄이는데 유용하게 이용될 수 있을 것으로 기대된다.
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