Hepatic stellate cells play essential roles in the development and regeneration of the liver. They are also implicated in liver cancer. However, what exactly is the function of these cells? This article will cover their physiological roles, mechanisms, and regulation.
The pathogenesis of hepatic steller cell inflammation has yet to be fully understood. It is thought to be caused by activating a particular cell type called myofibroblast. It has multiple functions, including migration, activation, and proliferation. Activated myofibroblasts can originate from bone marrow-derived fibrocytes, circulating mesenchymal cells, and resident liver cells.
Hepatic Stellate cell (HSC) plays a role in inflammatory and infectious diseases. They are thought to interact with various immune system cells, including cytokines and dendritic cells, and they can modulate their activity. They also play a role in regulating immune responses.
Chronic inflammation causes fibrosis in the liver, and it promotes the activation of hepatic stellate cells. Activation of hepatic stellate cells results in the production of downstream inflammatory mediators. These inflammatory mediators are induced by the TNF-a-dependent pathway. Interestingly, mice with knockout mutations in TNF-a, CD14, and TLR4 are protected from fibrosis. Knockout mice lack the genes that activate TLR4, NFB, and IRF3.
Hepatic stellate cells (HSC) play an essential role in liver fibrogenesis. These cells express toll-like receptors, which recognize pathogen-associated molecular patterns and initiate inflammatory responses. They produce collagen, which may be necessary for developing hepatic fibrosis. The earliest event in fibrosis development may be HSC activation.
HSCs also interact with immune cells. They produce several soluble factors that modulate the properties of immune cells. Inflammation-induced HSC releases various cytokines, including TNF and IL-1. These cytokines activate the transcription factor NF-kB in HSC and promote the survival of activated HSC and MFB.
HSC plays a vital role in liver homeostasis, inflammation, and immunity. Although most research on HSC has focused on its role in liver fibrogenesis, it has also been shown that these cells are central regulators of liver immunology. Understanding their functions as critical players in liver immunity will pave the way for new therapeutics.
Regulation of hepatic stellate cells is essential for the inflammatory response to liver disease. These cells secrete a cytokine called SDF1 and interact with endothelial cells through their SDF1a/CXCR4 receptor. They also regulate the proliferation of hepatoblast progenitor cells and recruit hematopoietic stem cells.
In addition to secreting soluble factors, HSCs interact with various immune cells to regulate their properties. Some of these interactions are discussed in detail in the text. For example, the exchange between HSC and multiple subpopulations of macrophages has been shown to have distinct consequences for the development and progression of liver disease.
Other studies have demonstrated that stellate cells in the liver have a role in liver regeneration. In addition to PH, toxins have also been shown to induce liver regeneration in zebrafish. Moreover, genetic tools have enabled the development of additional regeneration models, including the nitroreductase/metronidazole cell ablation system and morpholino-based knockdown of the mitochondrial import gene. In addition, high-throughput chemical screens have allowed researchers to identify drugs influencing stellate cells during liver regeneration.
HSCs play multiple roles in the liver, from facilitating the rapid exchange of blood molecules to degrading immunogenic molecules. They also produce a variety of polypeptide mediators, including erythropoietin. This hematopoietic growth factor may have beneficial actions during liver regeneration and injury.
These cells play a regulatory role during liver inflammation. Several studies have demonstrated that they are involved in the process by which hepatic stellate cells produce IFN-g and IL-4, two important mediators of inflammatory processes.
Inflammation in the liver is a dynamic network of reactions and should be viewed as such. Liver inflammation plays a vital role in liver function and homeostasis. Dysfunction of this inflammatory response will lead to liver dysfunction, cirrhosis, and chronic infection.
Inflammation in the liver is often accompanied by liver fibrosis, a disease characterized by excessive extracellular matrix production and impaired matrix degradation. Fibrosis of the liver can lead to cancer. Liver fibrosis is a standard pathological process in chronic liver disease and can be progressive and irreversible. Fibrosis is often triggered by an injury to the liver, which causes activation of HSCs and fibrogenesis. Natural killer cells, a vital component of the hepatic innate immune system, can relieve fibrosis by killing activated HSCs. However, current antifibrotic therapies cannot stop the progression of liver fibrosis in advanced stages.