Abstract
Cirrhosis, a late form of liver disease, is characterized by extensive scarring due to exacerbated secretion of extracellular matrix proteins by myofibroblasts that develop during this process. These myofibroblasts arise mainly from hepatic stellate cells (HSCs), liver-specific pericytes that become activated at the onset of liver injury. Consequently, HSCs tend to be viewed mainly as myofibroblast precursors in a fibrotic process driven by inflammation. Here, the molecular interactions between liver pericytes and inflammatory cells such as macrophages and neutrophils at the first moments after injury and during the healing process are brought into focus. Data on HSCs and pericytes from other tissues indicate that these cells are able to sense pathogen- and damage-associated molecular patterns and have an important proinflammatory role in the initial stages of liver injury. On the other hand, further data suggest that as the healing process evolves, activated HSCs play a role in skewing the initial proinflammatory (M1) macrophage polarization by contributing to the emergence of alternatively activated, pro-regenerative (M2-like) macrophages. Finally, data suggesting that some HSCs activated during liver injury could behave as hepatic progenitor or stem cells will be discussed.
Highlights
It is estimated that approximately two million deaths per year worldwide are due to liver diseases, including cirrhosis, viral hepatitis, and liver cancer [1]
In chronic liver diseases, which include viral infections, nonalcoholic steatohepatitis, alcoholic liver disease, and autoimmune diseases, necrosis and inflammation may progress to liver fibrosis and cirrhosis [5]
Kupffer cells (KCs), which account for nearly 30% of the non-parenchymal cells in the liver and around 85% of the tissue macrophages in the body, self-renew from liver-resident cells originated from the fetal yolk sack [21]
Summary
It is estimated that approximately two million deaths per year worldwide are due to liver diseases, including cirrhosis, viral hepatitis, and liver cancer [1]. Acute liver failure is a rare, life-threatening condition following severe hepatic injury. It can be caused by a variety of events leading to damage of liver cells, including viral infection and toxic drug effects. In chronic liver diseases, which include viral infections, nonalcoholic steatohepatitis, alcoholic liver disease, and autoimmune diseases, necrosis and inflammation may progress to liver fibrosis and cirrhosis [5]. Different cell types are involved in the processes of homeostasis, progression, and regression of liver diseases. Understanding their biology and function, as well as their interactions, is critically important for preventing and treating chronic liver diseases
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