Hepatic Inflammation and Fibrosis: Functional Links and Key Pathways

By E. Seki, Robert F. Schwabe. Hepatology, 2015

909 citations recorded by the source corpus.

Inflammation is one of the most characteristic features of chronic liver disease of viral, alcoholic, fatty, and autoimmune origin. Inflammation is typically present in all disease stages and associated with the development of fibrosis, cirrhosis, and hepatocellular carcinoma. In the past decade, numerous studies have contributed to improved understanding of the links between hepatic inflammation and fibrosis. Here, we review mechanisms that link inflammation with the development of liver fibrosis, focusing on the role of inflammatory mediators in hepatic stellate cell (HSC) activation and HSC survival during fibrogenesis and fibrosis regression. We will summarize the contributions of different inflammatory cells, including hepatic macrophages, T and B lymphocytes, natural killer cells and platelets, as well as key effectors, such as cytokines, chemokines, and damage‐associated molecular patterns. Furthermore, we will discuss the relevance of inflammatory signaling pathways for clinical liver disease and for the development of antifibrogenic strategies. (Hepatology 2015;61:1066–1079)

Subfields: Epidemiology, Hepatology

View Paper: https://www.semanticscholar.org/paper/6fff10ca11e9803d2f51fb2ac230b1b8e0ef5f9d

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In Epidemiology

1. M. Pinzani
2. M. Parola
3. Robert F. Schwabe

In Hepatology

1. M. Pinzani
2. M. Parola
3. Robert F. Schwabe
4. Le-xing Yu
5. S. Affò

Citations in the corpus

• Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues. (2019, background): “…α- SMA-positive cells that can originate from different mesenchymal precursor cells through a process of activation/transdifferentiation (Friedman, 2008; Novo et al., 2014; Lee et al., 2015; Seki and Schwabe, 2015; Trautwein et al., 2015; Wells and Schwabe, 2015; Tsuchida and Friedman, 2017).”
• The Role of Cancer-Associated Fibroblasts and Fibrosis in Liver Cancer (2016, background): “A large number of proinflammatory mediators, including IL-1, IL-6, TNF-α, lymphotoxin-β, and IL-17, are upregulated in the chronically injured liver and contribute to the development of HCC (25, 56, 57).”