Abstract
Most chronic liver diseases of all etiologies result in progressive liver fibrosis. Myofibroblasts produce the extracellular matrix, including type I collagen, which constitutes the fibrous scar in liver fibrosis. Normal liver has little type I collagen and no detectable myofibroblasts, but myofibroblasts appear early in experimental and clinical liver injury. The origin of the myofibroblast in liver fibrosis is still unresolved. The possibilities include activation of endogenous mesenchymal cells including fibroblasts and hepatic stellate cells, recruitment from the bone marrow, and transformation of epithelial or endothelial cells to myofibroblasts. In fact, the origin of myofibroblasts may be different for different types of chronic liver diseases, such as cholestatic liver disease or hepatotoxic liver disease. This review will examine our current understanding of the liver myofibroblast.
Highlights
Myofibroblasts are alpha smooth muscle actin positive cells that produce extracellular matrix proteins including fibrillar collagen
The myofibroblasts are imbedded in the fibrous scar
In both experimental and clinical liver fibrosis, there is a close correlation between the regression of liver fibrosis and the disappearance of these myofibroblasts
Summary
Myofibroblasts are alpha smooth muscle actin positive cells that produce extracellular matrix proteins including fibrillar collagen. Bone-marrow derived cells, consisting of fibrocytes and circulating mesenchymal cells, can be recruited to the injured liver to become myofibroblasts. Fibrocytes are a unique population of type I collagen expressing CD45+ cells derived from the bone marrow.
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