Abstract
Liver fibrosis is one of the risk factors for hepatocellular carcinoma (HCC) development. The staging of liver fibrosis can be evaluated only via a liver biopsy, which is an invasive procedure. Noninvasive methods for the diagnosis of liver fibrosis can be divided into morphological tests such as elastography and serum biochemical tests. Transient elastography is reported to have excellent performance in the diagnosis of liver fibrosis and has been accepted as a useful tool for the prediction of HCC development and other clinical outcomes. Two-dimensional shear wave elastography is a new technique and provides a real-time stiffness image. Serum fibrosis markers have been studied based on the mechanism of fibrogenesis and fibrolysis. In the healthy liver, homeostasis of the extracellular matrix is maintained directly by enzymes called matrix metalloproteinases (MMPs) and their specific inhibitors, tissue inhibitors of metalloproteinases (TIMPs). MMPs and TIMPs could be useful serum biomarkers for liver fibrosis and promising candidates for the treatment of liver fibrosis. Further studies are required to establish liver fibrosis-specific markers based on further clinical and molecular research. In this review, we summarize noninvasive fibrosis tests and molecular mechanism of liver fibrosis in current daily clinical practice.
Highlights
Hepatocellular carcinoma (HCC), one of the most common malignancies worldwide, is usually accompanied by advanced liver fibrosis or cirrhosis [1,2]
We previously reported that simple stromal injury mimics liver fibrosis with activation, of hepatic stellate cells (HSCs) and the production of transforming growth factor β1 (TGF-β1)
The development is depending the balance between causesproduction, In fibrosis turn, TGF-β1 activates hepatic stellate cell and on increases fibrolysis and fibrogenesis
Summary
Hepatocellular carcinoma (HCC), one of the most common malignancies worldwide, is usually accompanied by advanced liver fibrosis or cirrhosis [1,2]. C virus (HCV) is the leading cause of HCC in many countries [3,4,5]. Other major etiologies, such as alcoholic liver disease (ALD) and nonalcoholic steatohepatitis (NASH) have been increasing [6]. We previously reported that simple stromal injury mimics liver fibrosis with. HSC activation, of hepatic stellate cells (HSCs) and the production of transforming growth factor β1 (TGF-β1). We previously reported simple stromal injury mimics livermodel fibrosis[9]. With activation, turnover of ECM is regulated by enzymes called matrix metalloproteinase (MMPs) and their specific production, and collagen deposition using a mouse model [9].
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