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      Interaction of non-parenchymal hepatocytes in the process of hepatic fibrosis

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          Abstract

          Hepatic fibrosis (HF) is the process of fibrous scar formation caused by chronic liver injury of different etiologies. Previous studies have hypothesized that the activation of hepatic stellate cells (HSCs) is the central process in HF. The interaction between HSCs and surrounding cells is also crucial. Additionally, hepatic sinusoids capillarization, inflammation, angiogenesis and fibrosis develop during HF. The process involves multiple cell types that are highly connected and work in unison to maintain the homeostasis of the hepatic microenvironment, which serves a key role in the initiation and progression of HF. The current review provides novel insight into the intercellular interaction among liver sinusoidal endothelial cells, HSCs and Kupffer cells, as well as the hepatic microenvironment in the development of HF.

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          Macrophages: master regulators of inflammation and fibrosis.

          Thomas Wynn, Luke Barron (2010)
          Macrophages are found in close proximity with collagen-producing myofibroblasts and indisputably play a key role in fibrosis. They produce profibrotic mediators that directly activate fibroblasts, including transforming growth factor-beta1 and platelet-derived growth factor, and control extracellular matrix turnover by regulating the balance of various matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases. Macrophages also regulate fibrogenesis by secreting chemokines that recruit fibroblasts and other inflammatory cells. With their potential to act in both a pro- and antifibrotic capacity, as well as their ability to regulate the activation of resident and recruited myofibroblasts, macrophages and the factors they express are integrated into all stages of the fibrotic process. These various, and sometimes opposing, functions may be performed by distinct macrophage subpopulations, the identification of which is a growing focus of fibrosis research. Although collagen-secreting myofibroblasts once were thought of as the master "producers" of fibrosis, this review will illustrate how macrophages function as the master "regulators" of fibrosis. Copyright Thieme Medical Publishers.
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            Hepatic stellate cells as key target in liver fibrosis.

            Takaaki Higashi, Scott Friedman, Yujin Hoshida (2017)
            Progressive liver fibrosis, induced by chronic viral and metabolic disorders, leads to more than one million deaths annually via development of cirrhosis, although no antifibrotic therapy has been approved to date. Transdifferentiation (or "activation") of hepatic stellate cells is the major cellular source of matrix protein-secreting myofibroblasts, the major driver of liver fibrogenesis. Paracrine signals from injured epithelial cells, fibrotic tissue microenvironment, immune and systemic metabolic dysregulation, enteric dysbiosis, and hepatitis viral products can directly or indirectly induce stellate cell activation. Dysregulated intracellular signaling, epigenetic changes, and cellular stress response represent candidate targets to deactivate stellate cells by inducing reversion to inactivated state, cellular senescence, apoptosis, and/or clearance by immune cells. Cell type- and target-specific pharmacological intervention to therapeutically induce the deactivation will enable more effective and less toxic precision antifibrotic therapies.
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              Liver inflammation and fibrosis.

              Yukinori Koyama, David A. Brenner (2017)
              Chronic liver inflammation leads to fibrosis and cirrhosis, which is the 12th leading cause of death in the United States. Hepatocyte steatosis is a component of metabolic syndrome and insulin resistance. Hepatic steatosis may be benign or progress to hepatocyte injury and the initiation of inflammation, which activates immune cells. While Kupffer cells are the resident macrophage in the liver, inflammatory cells such as infiltrating macrophages, T lymphocytes, neutrophils, and DCs all contribute to liver inflammation. The inflammatory cells activate hepatic stellate cells, which are the major source of myofibroblasts in the liver. Here we review the initiation of inflammation in the liver, the liver inflammatory cells, and their crosstalk with myofibroblasts.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Med Rep
                Journal ID (iso-abbrev): Mol Med Rep
                Title: Molecular Medicine Reports
                Publisher: D.A. Spandidos
                ISSN (Print): 1791-2997
                ISSN (Electronic): 1791-3004
                Publication date (Print): May 2021
                Publication date (Electronic): 16 March 2021
                Publication date PMC-release: 16 March 2021
                Volume: 23
                Issue: 5
                Electronic Location Identifier: 364
                Affiliations
                [1 ]Medical College, China Three Gorges University, Yichang, Hubei 443002, P.R. China
                [2 ]Institute of Organ Fibrosis and Targeted Drug Delivery, China Three Gorges University, Yichang, Hubei 443002, P.R. China
                [3 ]Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang, Hubei 443002, P.R. China
                [4 ]The People's Hospital of China Three Gorges University, Yichang, Hubei 443000, P.R. China
                [5 ]The Yiling Hospital of Yichang, Yichang, Hubei 443100, P.R. China
                Author notes
                Correspondence to: Dr Yi-Ran Ni, Medical College, China Three Gorges University, 8 Daxue Road, Xiling, Yichang, Hubei 443002, P.R. China, E-mail: nyr1986@ 123456163.com
                Dr Wen-Bing Ai, The Yiling Hospital of Yichang, 31 Donghu Road, Yiling, Yichang, Hubei 443100, P.R. China, E-mail: 1043642574@ 123456qq.com
                Article
                Publisher ID: MMR-0-0-12003
                DOI: 10.3892/mmr.2021.12003
                PMC ID: 7986015
                PubMed ID: 33760176
                SO-VID: 8303353b-fc4b-4888-b142-9974bf114271
                Copyright © Copyright: © Cheng et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 03 October 2020
                Date accepted : 02 March 2021
                Funding
                Funded by: National Natural Science Foundation of China, open-funder-registry 10.13039/501100001809;
                Award ID: 81670555
                The present study was supported by the National Natural Science Foundation of China (grant no. 81670555).
                Categories
                Subject: Review

                Keywords: hepatic stellate cell,liver sinusoidal endothelial cell,kupffer cell,hepatic microenvironment,intercellular interaction
                Data availability:
                Keywords: hepatic stellate cell, liver sinusoidal endothelial cell, kupffer cell, hepatic microenvironment, intercellular interaction

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