Because the causes of the majority of liver diseases, such as chronic hepatitis B and autoimmune hepatitis, are difficult to remove, targeting the pathogenic mechanism underlying hepatic fibrosis may be an effective measure to intervene in the disease development process and treat hepatic fibrosis.
Currently, two main strategies are used for hepatic fibrosis treatment, eliminating pathogenic factors such as antivirus treatment and abstinence of drinking and decreasing synthesis and deposition of ECM in liver tissues.
Two major treatments are used against hepatic fibrosis: those that eliminate pathogenic factors that cause hepatic fibrosis (e.g., antiviral therapy and glucocorticoid treatment of autoimmune or alcoholic liver diseases) and those that target ECM accumulation by decreasing its synthesis and facilitating its degradation.
There were also indications of an increase in the opioid signaling within gastric mucosa that may results in a shift to proinflammatory environment within this organ and contribute to systemic inflammation and the pathogenic processes in hepatic parenchyma.
The main pathogenic factors that induce hepatic fibrosis include chronic hepatitis virus (i.e., HBV and HCV) and parasite infection (e.g., schistosomes), alcoholic liver disease, fatty liver disease, cholestasis, drug-induced liver injury, and autoimmune hepatitis.
From the quantitative standpoint, increased hepatic glucose production represents the major pathogenic disturbance responsible for hyperglycemia in DKA (34).
Accumulating evidence from murine models demonstrated that the infiltration of monocytes into the liver is a major pathogenic factor for chronic hepatic inflammation and fibrosis [ 3- 6].
The reason why the incidence of ICC in patients of viral hepatitis B or C is substantially lower than that of HCC if both arise from the same hepatic progenitor cells with a common pathogenic process remains unknown.
Together, these results suggest that regulation of hepatic lipid concentration may be an important pathogenic site that is modified by CRF independent of standard measures of adiposity.
Hepatic gene transfer as a means of reversing pathogenic antibody formation is also applicable to lysosomal storage disorders as shown for Pompe disease (Sun et al, 2010).
