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- Debanjan Dhar
- Department of Medicine, University of California San Diego, La Jolla, CA 92093, USA
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- Jacopo Baglieri
- Department of Medicine, University of California San Diego, La Jolla, CA 92093, USA
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- Tatiana Kisseleva
- Department of Surgery, University of California San Diego, La Jolla, CA 92093, USA
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- David A Brenner
- Department of Medicine, University of California San Diego, La Jolla, CA 92093, USA
説明
<jats:p>Hepatic fibrogenesis is a pathophysiological outcome of chronic liver injury hallmarked by excessive accumulation of extracellular matrix proteins. Fibrosis is a dynamic process that involves cross-talk between parenchymal cells (hepatocytes), hepatic stellate cells, sinusoidal endothelial cells and both resident and infiltrating immune cells. In this review, we focus on key cell-types that contribute to liver fibrosis, cytokines, and chemokines influencing this process and what it takes for fibrosis to regress. We discuss how mitochondria and metabolic changes in hepatic stellate cells modulate the fibrogenic process. We also briefly review how the presence of fibrosis affects development of hepatocellular carcinoma.</jats:p><jats:sec><jats:title>Impact statement</jats:title><jats:p>Advanced liver fibrosis results in cirrhosis, portal hypertension, and liver failure and often requires liver transplantation. Advanced liver fibrosis and cirrhosis are also major risk factors for hepatocellular carcinoma (HCC). Hepatic stellate cells (HSCs) play a pivotal role in the pathogenesis of liver fibrosis. In this review, we summarize the basic mechanisms that influence liver fibrosis development and how oxidative stress, mitochondrial dysfunction, and metabolic remodeling modulate HSC activation and indicate areas of potential therapeutic intervention.</jats:p></jats:sec>
収録刊行物
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- Experimental Biology and Medicine
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Experimental Biology and Medicine 245 (2), 96-108, 2020-01
Frontiers Media SA