Article
Immunology
Fangming Yang, Heng Li, Yanmin Li, Yaokun Hao, Chenxiao Wang, Pan Jia, Xinju Chen, Suping Ma, Zhun Xiao
Summary: Hepatic fibrosis is a dynamic pathological process characterized by the accumulation of extra cellular matrix in chronic liver diseases, with activation of hepatic stellate cells (HSCs) playing a central role. Communication between hepatocytes and surrounding cells influences the activation of HSCs and the progression of fibrosis, highlighting the complexity and plasticity of HSC activation.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Review
Oncology
Yang Zhang, Yuan Wu, Wenjuan Shen, Bingyu Wang, Xingxing Yuan
Summary: Liver fibrosis is a common pathological process in chronic liver diseases, which can progress to irreversible cirrhosis and cancer. Hepatic stellate cells are activated and produce collagen in response to liver injury, triggering the initiation and progression of fibrosis. Natural killer cells, as a key component of hepatic innate immunity, can alleviate fibrosis by killing activated hepatic stellate cells. Current antifibrotic interventions have improved fibrosis, but cannot halt its progression in the advanced stage. Understanding the interaction between natural killer cells and hepatic stellate cells may provide clues for the pathogenesis and potential therapies for advanced liver fibrosis.
MOLECULAR MEDICINE REPORTS
(2022)
Review
Immunology
Wei Du, Lin Wang
Summary: This article reviews the key role of crosstalk between liver sinusoidal endothelial cells (LSECs) and hepatic microenvironment in the progression of NASH to liver fibrosis, and discusses promising therapeutic strategies targeting LSECs.
FRONTIERS IN IMMUNOLOGY
(2022)
Review
Gastroenterology & Hepatology
Leke Wiering, Pallavi Subramanian, Linda Hammerich
Summary: Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease with a wide range of severity, from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). NASH can lead to liver fibrosis, cirrhosis, and hepatocellular carcinoma, making hepatic fibrosis an important predictor of outcomes. Recent advancements in understanding the activation and inactivation of hepatic stellate cells, which drive fibrosis development, have shed light on the disease progression in NAFLD/NASH.
CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
(2023)
Article
Chemistry, Multidisciplinary
Xiaoping Wu, Lingling Shu, Zixuan Zhang, Jingjing Li, Jiuyu Zong, Lai Yee Cheong, Dewei Ye, Karen S. L. Lam, Erfei Song, Cunchuan Wang, Aimin Xu, Ruby L. C. Hoo
Summary: Liver fibrosis results in significant changes in the liver microenvironment, which promotes disease progression. The study demonstrates that increased expression of adipocyte fatty acid binding protein (A-FABP) in liver sinusoidal endothelial cells (LSECs) plays a crucial role in promoting liver fibrosis in mice. A-FABP activates signaling pathways that lead to liver fibrosis progression, suggesting that targeting A-FABP may be a potential therapeutic approach against liver fibrosis.
Article
Cell Biology
Yu Peng, Zedong Li, Sheng Chen, Jun Zhou
Summary: Liver fibrogenesis is a dynamic cellular and tissue process that can lead to cirrhosis, liver cancer, and liver failure. This study found that exosomes secreted from activated hepatic stellate cells can promote M1 polarization of macrophages, with DHFR playing a crucial role in this process. The results suggest a significant crosstalk between HSCs activation and macrophage polarization in liver fibrosis.
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
(2021)
Review
Medicine, Research & Experimental
Yuan Wei, Wang Bingyu, Yang Lei, Yuan Xingxing
Summary: Liver fibrosis is a common pathological change in chronic liver diseases, and this review focuses on the role and potential of NK cells in controlling fibrosis.
EXPERIMENTAL BIOLOGY AND MEDICINE
(2022)
Article
Biochemistry & Molecular Biology
Aiting Yang, Xuzhen Yan, Hufeng Xu, Xu Fan, Mengyang Zhang, Tao Huang, Weiyu Li, Wei Chen, Jidong Jia, Hong You
Summary: The deficiency of HSCs-specific Loxl1 can prevent CCl4-induced hepatic fibrosis and reduce fibrosis and inflammation in liver tissue, with ITGA8/FAK/PI3K/AKT/HIF1a being essential for the function and expression of LOXL1. The study suggests novel mechanisms and potential targets for the treatment of fibrosis in the future.
Review
Biochemistry & Molecular Biology
Chanbin Lee, Minju Kim, Jinsol Han, Myunghee Yoon, Youngmi Jung
Summary: Liver fibrosis is a common feature of chronic liver disease and regulating HSC activation is crucial for its treatment. MSCs interact directly with immune cells, HSCs, and hepatocytes to secrete modulators and reduce liver fibrosis. Both MSC itself and MSC modulators have shown anti-fibrotic functions, but the underlying mechanism is yet to be established.
Article
Chemistry, Multidisciplinary
Mahmoud A. Younis, Yusuke Sato, Yaser H. A. Elewa, Hideyoshi Harashima
Summary: This article reports a novel strategy for treating liver fibrosis by reprogramming activated Hepatic Stellate Cells (aHSCs) into quiescent Hepatic Stellate Cells (qHSCs) using siRNA-loaded lipid nanoparticles (LNPs). The optimized LNPs enable ligand-free, selective, and potent siRNA delivery to aHSCs, resulting in the reversal of liver fibrosis and restoration of normal liver function in mice. This scalable and ligand-free platform has potential for clinical translation.
JOURNAL OF CONTROLLED RELEASE
(2023)
Article
Nanoscience & Nanotechnology
Shiqin Luo, Yuping Yang, Ting Zhao, Rongping Zhang, Changlong Fang, Yan Li, Zhirong Zhang, Tao Gong
Summary: Activated hepatic stellate cells (aHSCs) play a critical role in liver fibrosis. The study introduces a nano platform called silibinin albumin nanocrystals (SLB-HSA NCs) for targeted therapy of liver fibrosis. The SLB-HSA NCs demonstrated a uniform particle size distribution of approximately 60 nm, high loading efficiency, and increased cellular uptake by aHSCs through SPARC-mediated endocytosis. In pharmacokinetic study, SLB-HSA NCs exhibited enhanced bioavailability compared with free SLB. Furthermore, they showed significant antifibrotic effects in hepatic fibrosis mice.
ACS APPLIED MATERIALS & INTERFACES
(2023)
Article
Biochemistry & Molecular Biology
Tian-tian Sun, Xu-ling Liu, Guang-yue Yang, Wei Zhang, Le Tao, Wen-ting Ma, Liu Wu, Qigen Li, Cheng Liu
Summary: This study found that patients with hepatic fibrosis had significantly higher levels of neurokines, and that hepatic stellate cells interact with nerves to produce neurogenic substances that promote liver fibrosis.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Biochemistry & Molecular Biology
Tian-Tian Sun, Xu-Ling Liu, Guang-Yue Yang, Wei Zhang, Le Tao, Wen-Ting Ma, Liu Wu, Qigen Li, Cheng Liu
Summary: This study aimed to investigate the changes in nerve factors and neurokines and their relation to hepatic stellate cells (HSCs) in liver fibrosis. The results showed significantly increased expression levels of neurokines in both human and animal liver fibrosis. It was also observed that there is interaction between nerve cells and HSCs, and nerve cells produce neurogenic substances that promote liver fibrosis and HSC activation.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Biochemistry & Molecular Biology
Maximilian Schinagl, Tamara Tomin, Juergen Gindlhuber, Sophie Honeder, Raphael Pfleger, Matthias Schittmayer, Michael Trauner, Ruth Birner-Gruenberger
Summary: This study investigated the activation of hepatic stellate cells (HSC) through an increase in growth medium serum concentration, revealing cellular processes involved in HSC transformation. Activated HSC showed increased production of ribosomal proteins and proteins related to migration and cell cycle control, along with a decrease in cholesterol and fatty acid biosynthesis proteins. The findings provide insights into HSC activation characteristics and present a accessible model for studying HSC activation.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Neurosciences
Dakota R. Kamm, Kyle S. McCommis
Summary: Hepatic stellate cells (HSCs) play critical roles in the normal liver and in response to injury. They are activated during liver injury and produce extracellular matrix in liver fibrosis. In the absence of injury, HSCs are in a quiescent state and store retinoids or vitamin A-containing metabolites. They also enhance the inflammatory response and express growth factors crucial for liver development and regeneration. Recent studies have identified diverse phenotypic alterations and unique subpopulations of HSCs.
JOURNAL OF PHYSIOLOGY-LONDON
(2022)
