Abstract
Liver can get damaged from various injurious factors which, when acting chronically can result in liver injury and inflammation. This leads to repair, healing, and fibrosis, which ultimately can result into cirrhosis. Cirrhosis has its consequences and can result in hepatic insufficiency and portal hypertension, which in turn lead to porto-systemic encephalopathy, gastrointestinal bleeding, ascites, renal dysfunction, and ultimately can lead to hepatocellular carcinoma and death.1 Various factors like viruses, toxic substances, drugs, auto immune hepatitis, steatosis and alcohol can result in liver injury. In our scenario, hepatitis B and C are the commonest causes of liver fibrosis and cirrhosis.

Multiple mechanisms have been described which lead to liver fibrosis. The central factor is activation of hepatic stellate cells, which occurs from multiple reasons, which cause the quiescent cell to become activated. Injury to hepatocytes and cholangiocytes stimulates hepatic stellates cells via various cytokines and thus these cells become activated.2 When activated, these cells start poring extra cellular matrix, which result in deposition of fibrin resulting in fibrosis (fibrogenesis).3 Stellate cells result in proliferation, inflammation, contractility, chemotaxis, altered matrix degradation and retinoid loss.2 Hepatitis B virus X protein (HBx), large isoform of hepatitis delta antigen (LHDAg) and hepatitis C virus derived proteins have been documented to induce stellate cell activation.2 With ongoing insult and on poring of extra cellular matrix in the sinusides, this progresses to high grade fibrosis and cirrhosis.

Key words: Hepatic fibrosis, cirrhosis, fibrogenesis, stellate cells.