scholarly journals Current and Emerging Approaches for Hepatic Fibrosis Treatment

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jingguo Li ◽  
Biguang Tuo
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Fibrosis ◽  
Chronic Liver ◽  
Chronic Liver Injury ◽  
Major Health ◽  
Health Burden ◽  
Liver Disease Progression ◽  
Tremendous Progress ◽  
Key Factor ◽  
Novel Approaches

Liver fibrosis resulting from chronic liver injury is a key factor to develop liver cirrhosis and risk of hepatocellular carcinoma (HCC) which are major health burden worldwide. Therefore, it is necessary for antifibrotic therapies to prevent chronic liver disease progression and HCC development. There has been tremendous progress in understanding the mechanisms of liver fibrosis in the last decade, which has created new opportunities for the treatment of this condition. In this review, we aim to make an overview on information of different potential therapies (drug treatment, cell therapy, and liver transplantation) for the liver fibrosis and hope to provide the therapeutic options available for the treatment of liver fibrosis and discuss novel approaches.

scholarly journals The roles and mechanisms of hypoxia in liver fibrosis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jingyao Cai ◽  
Min Hu ◽  
Zhiyang Chen ◽  
Zeng Ling
Keyword(s):  
Quality Of Life ◽  
Liver Fibrosis ◽  
Theoretical Basis ◽  
Liver Diseases ◽  
Molecular Mechanisms ◽  
Clinical Intervention ◽  
Chronic Liver Injury ◽  
Key Factor

AbstractLiver fibrosis occurs in response to any etiology of chronic liver injury. Lack of appropriate clinical intervention will lead to liver cirrhosis or hepatocellular carcinoma (HCC), seriously affecting the quality of life of patients, but the current clinical treatments of liver fibrosis have not been developed yet. Recent studies have shown that hypoxia is a key factor promoting the progression of liver fibrosis. Hypoxia can cause liver fibrosis. Liver fibrosis can, in turn, profoundly further deepen the degree of hypoxia. Therefore, exploring the role of hypoxia in liver fibrosis will help to further understand the process of liver fibrosis, and provide the theoretical basis for its diagnosis and treatment, which is of great significance to avoid further deterioration of liver diseases and protect the life and health of patients. This review highlights the recent advances in cellular and molecular mechanisms of hypoxia in developments of liver fibrosis.

Cellular Mechanisms of Tissue Fibrosis. 5. Novel insights into liver fibrosis

2013 ◽  
Vol 305 (8) ◽  
pp. C789-C799 ◽  
Author(s):  
Ariane Mallat ◽  
Sophie Lotersztajn
Keyword(s):  
Liver Fibrosis ◽  
Liver Injury ◽  
Cell Injury ◽  
Parenchymal Cell ◽  
Chronic Liver ◽  
Special Focus ◽  
Chronic Liver Injury ◽  
Cellular Mechanisms ◽  
Extracellular Matrix Components ◽  
Liver Fibrogenesis

Liver fibrosis is the common scarring reaction associated with chronic liver injury that results from prolonged parenchymal cell injury and/or inflammation. The fibrogenic response is characterized by progressive accumulation of extracellular matrix components enriched in fibrillar collagens and a failure of matrix turnover. This process is driven by a heterogeneous population of hepatic myofibroblasts, which mainly derive from hepatic stellate cells and portal fibroblasts. Regression of fibrosis can be achieved by the successful control of chronic liver injury, owing to termination of the fibrogenic reaction following clearance of hepatic myofibroblasts and restoration of fibrolytic pathways. Understanding of the complex network underlying liver fibrogenesis has allowed the identification of a large number of antifibrotic targets, but no antifibrotic drug has as yet been approved. This review will highlight recent advances regarding the mechanisms that regulate liver fibrogenesis and fibrosis regression, with special focus on novel signaling pathways and the role of inflammatory cells. Translation of these findings to therapies will require continued efforts to develop multitarget therapeutic approaches that will improve the grim prognosis of liver cirrhosis.

scholarly journals Perioperative exercise capacity in chronic liver injury patients with hepatocellular carcinoma undergoing hepatectomy

PLoS ONE ◽  
2019 ◽  
Vol 14 (8) ◽  
pp. e0221079 ◽  
Author(s):  
Masaki Kaibori ◽  
Kosuke Matsui ◽  
Kengo Yoshii ◽  
Morihiko Ishizaki ◽  
Junji Iwasaka ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Injury ◽  
Exercise Capacity ◽  
Chronic Liver ◽  
Chronic Liver Injury

scholarly journals Assessment of preoperative exercise capacity in hepatocellular carcinoma patients with chronic liver injury undergoing hepatectomy

2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Masaki Kaibori ◽  
Morihiko Ishizaki ◽  
Kosuke Matsui ◽  
Richi Nakatake ◽  
Tatsuma Sakaguchi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Injury ◽  
Exercise Capacity ◽  
Chronic Liver ◽  
Chronic Liver Injury ◽  
Preoperative Exercise

scholarly journals Liver fibrosis is driven by protease‐activated receptor‐1 expressed by hepatic stellate cells in experimental chronic liver injury

2020 ◽  
Vol 4 (5) ◽  
pp. 906-917
Author(s):  
Lauren G. Poole ◽  
Asmita Pant ◽  
Holly M. Cline‐Fedewa ◽  
Kurt J. Williams ◽  
Bryan L. Copple ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Liver Injury ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Chronic Liver ◽  
Chronic Liver Injury ◽  
Protease Activated Receptor 1

scholarly journals Hepatic Stellate Cell–Macrophage Crosstalk in Liver Fibrosis and Carcinogenesis

2020 ◽  
Vol 40 (03) ◽  
pp. 307-320
Author(s):  
Michitaka Matsuda ◽  
Ekihiro Seki
Keyword(s):  
Liver Fibrosis ◽  
Liver Injury ◽  
Cell Activation ◽  
Stellate Cell ◽  
Tumor Development ◽  
Mesenchymal Cell ◽  
Chronic Liver ◽  
Health Concern ◽  
Chronic Liver Injury ◽  
Fibrotic Liver

AbstractChronic liver injury due to viral hepatitis, alcohol abuse, and metabolic disorders is a worldwide health concern. Insufficient treatment of chronic liver injury leads to fibrosis, causing liver dysfunction and carcinogenesis. Most cases of hepatocellular carcinoma (HCC) develop in the fibrotic liver. Pathological features of liver fibrosis include extracellular matrix (ECM) accumulation, mesenchymal cell activation, immune deregulation, and angiogenesis, all of which contribute to the precancerous environment, supporting tumor development. Among liver cells, hepatic stellate cells (HSCs) and macrophages play critical roles in fibrosis and HCC. These two cell types interplay and remodel the ECM and immune microenvironment in the fibrotic liver. Once HCC develops, HCC-derived factors influence HSCs and macrophages to switch to protumorigenic cell populations, cancer-associated fibroblasts and tumor-associated macrophages, respectively. This review aims to summarize currently available data on the roles of HSCs and macrophages in liver fibrosis and HCC, with a focus on their interaction.

LC3-associated phagocytosis protects against inflammation and liver fibrosis via immunoreceptor inhibitory signaling

2020 ◽  
Vol 12 (539) ◽  
pp. eaaw8523 ◽  
Author(s):  
JingHong Wan ◽  
Emmanuel Weiss ◽  
Sanae Ben Mkaddem ◽  
Morgane Mabire ◽  
Pierre-Marie Choinier ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Liver Injury ◽  
Systemic Inflammation ◽  
Multiorgan Failure ◽  
Chronic Liver ◽  
Human Monocytes ◽  
Macrophage Phenotype ◽  
Chronic Liver Injury ◽  
Inflammatory Profile ◽  
Inhibitory Signaling

Sustained hepatic and systemic inflammation, particularly originating from monocytes/macrophages, is a driving force for fibrosis progression to end-stage cirrhosis and underlies the development of multiorgan failure. Reprogramming monocyte/macrophage phenotype has emerged as a strategy to limit inflammation during chronic liver injury. Here, we report that LC3-associated phagocytosis (LAP), a noncanonical form of autophagy, protects against hepatic and systemic inflammation during chronic liver injury in rodents, with beneficial antifibrogenic effects. LAP is enhanced in blood and liver monocytes from patients with fibrosis and cirrhosis. Pharmacological inhibition of LAP components in human monocytes from patients with cirrhosis or genetic disruption of LAP in mice with chronic liver injury exacerbates both the inflammatory signature in isolated human monocytes and the hepatic inflammatory profile in mice, resulting in enhanced liver fibrosis. Mechanistically, patients with cirrhosis showed increased monocyte expression of Fc fragment of IgG receptor IIA (FcγRIIA) and enhanced engulfment of immunoglobulin G in LC3+ phagosomes that triggers an FcγRIIA/Src homology region 2 domain–containing phosphatase-1 (SHP-1) inhibitory immunoreceptor tyrosine-based activation motif (ITAMi) anti-inflammatory pathway. Mice overexpressing human FcγRIIA in myeloid cells show enhanced LAP in response to chronic liver injury and resistance to inflammation and liver fibrosis. Activation of LAP is lost in monocytes from patients with multiorgan failure and restored by specifically targeting ITAMi signaling with anti-FcγRIIA F(ab′)2 fragments, or with intravenous immunoglobulin (IVIg). These data suggest the existence of an ITAMi-mediated mechanism by which LAP might protect against inflammation. Sustaining LAP may open therapeutic perspectives for patients with chronic liver disease.

Aspirin induces autophagy and alleviates liver fibrosis by reducing oxidative stress and inflammation in mice model of chronic liver injury

2020 ◽  
Vol 73 ◽  
pp. S527
Author(s):  
Adil Bhat ◽  
Sudrishti Chaudhary ◽  
Gaurav Yadav ◽  
Anupama Parasar ◽  
Chhagan Bihari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Chronic Liver ◽  
Mice Model ◽  
Chronic Liver Injury
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