Liver fibrosis is not an independent disease but rather a histological change caused by liver inflammation. Liver damage causes liver stellate cells to become overactive and triggers increase of extra cellular matrix (ECM) synthesis. When above normal amounts of collagen fiber deposits in the extra-cellular spaces of the liver cells, this causes liver cells to lose blood infusion and promotes hardening.

Chronic viral hepatitis B and C are the most common causes of liver fibrosis. During the chronic hepatitis course, fibrosis is a part of the inflammation activities. In the fibrosis stage, there is no lobular regeneration and this distinguishes it from cirrhosis. When fibrosis advances to cause separations (or bridging) between the portal areas, the center vein, and the formation of pseudo-lobule, fibrosis enters the cirrhosis.

Histological (biopsy) diagnosis classifies the severity of fibrosis into five general stages.  S-0 to S-4. Stage S-0 denotes no distinguishable fibrosis activity. S4 is considered cirrhosis.

In between, S1 is a mild fibrosis seen at the portal area. S2 is a moderate stage of fibrosis, between portal areas, but without the destruction of the liver lobular structure. S3 is severe fibrosis.  At this stage, there is fibrostic bridging between portal areas and center veins. At S4, in addition to S3's changes, there are pseudo-lobules formed. S4 is the cirrhosis stage and approximately 15 to 20% of HCV patients may progress to stage 4.

Liver fibrosis is the net result of the imbalance between the collagen fiber synthesis and decomposition. When fiber synthesis is very active and the decomposition process is suppressed, fibrosis will progress. Vise versa, fibrosis can be reversed if the causal factor, liver inflammation, can be controlled. When fibers form at the early stage, it can be decomposed with water or weak acid. These are soluble fibers. Older fibers deposited for long time, becomes thicker and harder. These cannot be decomposed by water or weak acids and only collagen enzymes can decompose them.  With anti-fibrosis treatment, there it is possible to enhance the activities of collagen enzymes and to promote the decomposition of the fibers, reducing ECM.