Hepatic Fibrosis

Deadline for manuscript submissions: 31 October 2023.

Topic Editor (1)

Ralf  Weiskirchen
Prof. Ralf Weiskirchen 
Institute of Molecular Pathobiochemistry, Experimental Gene Therapy and Clinical Chemistry (IFMPEGKC), RWTH University Hospital Aachen, Aachen, 52074, Germany
Interests: Liver Disease; Fibrosis; Biomarker; Cytokines; Chemokines; Translational medicine

Topic Collection Information

Topic Introduction and Keyords
Hepatic fibrosis is the result of a chronic would-healing process that is associated with excessive connective tissue accumulation and portal hypertension. It is further accompanied by progressive architectural tissue remodeling and progressive loss of liver function. Irrespective of the underlying pathogenic cause of liver fibrogenesis, it is initiated by an inflammatory response and a systemic mobilization of endocrine and neurological mediators that stimulate the proliferation and synthetic capacity of different matrix-producing cell populations. The process is further characterized by reactive oxygen species formation, endoplasmic reticulum stress increased intestinal permeability, biochemical alterations of mitochondrial function, and microbiota changes.
In this Topic Collection of Fibrosis, I invite you to contribute original research articles, brief reports systematic reviews, systemic and shorter perspectives, opinions, and expert perspectives on all aspects related to the theme of “Hepatic Fibrosis”. Relevant topics refer to but are not limited to:
•    Cytokines and chemokines
•    Experimental models of hepatic fibrosis
•    Extracellular matrix
•    Hepatic inflammation
•    Fibrosis, cirrhosis, and hepatocellular carcinoma
•    Steatosis and fatty liver disease (NASH/NAFLD/MAFLD)
•    Alcohol in hepatic disease
•    Hepatitis
•    Microbiota
•    Liver imaging techniques
•    Translational medicine
•    Clinical studies on hepatic therapy

Published Papers (1 papers)

Article

16 September 2023

Hepatic Lysosomal Enzyme Activity in Primary Biliary Cholangitis

Background: Lysosomal enzymes are implicated in autophagy and senescence. Hepatic lysosomal enzymes have not been studied in Primary Biliary Cholangitis (PBC). We therefore quantified the activities of lysosomal hydrolases in liver tissue of PBC patients. Methods: We compared enzyme activities in liver tissue from PBC patients with normal livers. Alcoholic liver disease and chronic viral disease served as disease controls. Results: Cathepsin B1 was significantly increased in early PBC (225.1 ± 18.06 mean ± SD, p < 0.0001) and reduced in later stages (66.5 ± 9.7, p = 0.004, controls 130.4 ± 14.9). It was reduced in patients with extensive fibrosis such as alcoholic and viral cirrhosis (p < 0.01 and p = 0.004 respectively) but not in chronic hepatitis. Cathepsin D was increased in early PBC (39 × 103 ± 4.8 SD, p < 0.0001) and less so in later stages (20.1 × 103 ± 3.9, p = 0.05, controls 14.1 × 103 ± 2.9). It was also increased in the presence of histological necro-inflammation in hepatitis. Treatment with ursodeoxycholate (UDCA) restored the abnormal values of enzymes in PBC. Lipid hydrolases mostly paralleled the changes of Cathepsins. Sequential measurements in serum of patients with acute alcoholic hepatitis showed that cathepsin B1 gradually decreases, and esterases increase as aminotransferases improve. Conclusions: The increased activity of lysosomal enzymes in early PBC are possibly on line with increased senescence. Treatment with UDCA restores abnormal values. In chronic liver disease, Cathepsin B1 reduction is associated with fibrosis and increased cathepsin D with necro-inflammation. Abnormalities of lysosomal enzymes indicate impairment of the final stage of autophagy in chronic liver disease.

Ioannis Tsomidis
Georgios Notas
Argyro Voumvouraki
Dimitrios Samonakis
Mairi Koulentaki
Elias Kouroumalis*
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