Special Issue on "Cellular and Molecular Mechanisms Underlying the Pathogenesis of Hepatic Fibrosis"

Abstract

This Special issue contains 48 contributions highlighting novel findings and current concepts in basic and clinical liver fibrosis research. These articles emphasize issues on pathogenesis, cellular mediators, modulators, molecular pathways, disease-specific therapies, scoring systems, as well as novel preclinical animal models for the study of liver fibrogenesis. This editorial aims to briefly summarize the content of these papers.

Figure 1

Topics covered in this Special Issue. The Special Issue “Cellular and Molecular Mechanisms Underlying the Pathogenesis of Hepatic Fibrosis” includes 26 original and 22 review articles written by 319 authors from 25 countries. These contributions discuss aspects of basic, clinical and translational research in the field of liver fibrosis. Special emphasis is given on the themes listed. Abbreviations used are: ADAM, a disintegrin and metalloproteinase; Akt1/2, serine/threonine-protein kinase 1/2; BM, bone marrow; BMP-8B, bone morphogenetic protein-8B; DAMPs; damage-associated molecular patterns; FHL2, four-and-a-half LIM-domain protein 2; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HFE, gene encoding the homeostatic iron regulator; HSC, hepatic stellate cell(s); iPla2β, Phospholipase A2; MFB, myofibroblast(s); mtDNA, mitochondrial DNA; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatophepatitis; NLRP3, NLR family pyrin domain-containing 3; Pin1, peptidyl-prolyl cis/trans isomerase, NIMA-interacting 1; P2X7R, purinergic receptor P2X; RUNX1, Runt-related transcription factor 1; TGR5, Takeda G-protein-coupled receptor 5; Ubl-PTMs, Ubiquitin-like post-translational modifications.